TY  - JOUR
AU  - Martinović, Vesna
AU  - Arambašić Jovanović, Jelena
AU  - Bogojević, Desanka
AU  - Ivanović, Anđelija
AU  - Otašević, Vesna
AU  - Stančić, Ana
AU  - Grigorov, Ilijana
PY  - 2020
UR  - http://www.doiserbia.nb.rs/Article.aspx?ID=0354-46642000049M
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4103
UR  - http://www.serbiosoc.org.rs/arch/index.php/abs/article/view/5980
AB  - Haptoglobin (Hp) is a hemoglobin-binding protein that prevents free hemoglobin-induced tissue oxidative damage. In streptozotocin-induced diabetic rats, the initial elevation of Hp expression in the serum and liver tends to decrease with diabetes progression, contributing to increased oxidative stress. Glucose toxicity and diabetic complications are closely related to increased modification of nucleocytoplasmic proteins by O-linked-N-acetylglucosamine (O-GlcNAc). We examined the contribution of O-GlcNAcylation of NF-κB p65 to changes in liver Hp expression in diabetic rats. WGA-affinity chromatography revealed a progressive increase in O-GlcNAcylation in nuclear NF-κB p65 during eight weeks of diabetes. DNA-affinity chromatography followed by immunoblot analysis revealed that decreased Hp expression at 4 and 8 weeks of diabetes was accompanied by the absence of Hp gene hormone-responsive element (HRE) occupancy with NF-κB p65, low occupancy with glucocorticoid receptor (GR), and almost no changes in STAT3 occupancy compared to 2 weeks, when Hp expression was highest. Coimmunoprecipitation experiments indicate that these events were the result of impaired NF-κB p65/STAT3 and GR/STAT3 interactions. Results suggest that the attenuation of Hp expression associated with diabetes was at least in part the result of O-GlcNAcylation of NF-κB p65, which prevents the formation of an effective transcription initiation complex on the Hp gene promoter.
PB  - Contribution of O-GlcNAc modification of NF-κB p65 in the attenuation of diabetes-induced haptoglobin expression in rat liver
T2  - Archives of Biological Sciences
T1  - Contribution of O-GlcNAc modification of NF-κB p65 in the attenuation of diabetes-induced haptoglobin expression in rat liver
IS  - 4
VL  - 72
DO  - 10.2298/ABS200928049M
SP  - 555
EP  - 565
ER  - 

@article{
author = "Martinović, Vesna and Arambašić Jovanović, Jelena and Bogojević, Desanka and Ivanović, Anđelija and Otašević, Vesna and Stančić, Ana and Grigorov, Ilijana",
year = "2020",
abstract = "Haptoglobin (Hp) is a hemoglobin-binding protein that prevents free hemoglobin-induced tissue oxidative damage. In streptozotocin-induced diabetic rats, the initial elevation of Hp expression in the serum and liver tends to decrease with diabetes progression, contributing to increased oxidative stress. Glucose toxicity and diabetic complications are closely related to increased modification of nucleocytoplasmic proteins by O-linked-N-acetylglucosamine (O-GlcNAc). We examined the contribution of O-GlcNAcylation of NF-κB p65 to changes in liver Hp expression in diabetic rats. WGA-affinity chromatography revealed a progressive increase in O-GlcNAcylation in nuclear NF-κB p65 during eight weeks of diabetes. DNA-affinity chromatography followed by immunoblot analysis revealed that decreased Hp expression at 4 and 8 weeks of diabetes was accompanied by the absence of Hp gene hormone-responsive element (HRE) occupancy with NF-κB p65, low occupancy with glucocorticoid receptor (GR), and almost no changes in STAT3 occupancy compared to 2 weeks, when Hp expression was highest. Coimmunoprecipitation experiments indicate that these events were the result of impaired NF-κB p65/STAT3 and GR/STAT3 interactions. Results suggest that the attenuation of Hp expression associated with diabetes was at least in part the result of O-GlcNAcylation of NF-κB p65, which prevents the formation of an effective transcription initiation complex on the Hp gene promoter.",
publisher = "Contribution of O-GlcNAc modification of NF-κB p65 in the attenuation of diabetes-induced haptoglobin expression in rat liver",
journal = "Archives of Biological Sciences",
title = "Contribution of O-GlcNAc modification of NF-κB p65 in the attenuation of diabetes-induced haptoglobin expression in rat liver",
number = "4",
volume = "72",
doi = "10.2298/ABS200928049M",
pages = "555-565"
}

Martinović, V., Arambašić Jovanović, J., Bogojević, D., Ivanović, A., Otašević, V., Stančić, A.,& Grigorov, I.. (2020). Contribution of O-GlcNAc modification of NF-κB p65 in the attenuation of diabetes-induced haptoglobin expression in rat liver. in Archives of Biological Sciences
Contribution of O-GlcNAc modification of NF-κB p65 in the attenuation of diabetes-induced haptoglobin expression in rat liver., 72(4), 555-565.
https://doi.org/10.2298/ABS200928049M

Martinović V, Arambašić Jovanović J, Bogojević D, Ivanović A, Otašević V, Stančić A, Grigorov I. Contribution of O-GlcNAc modification of NF-κB p65 in the attenuation of diabetes-induced haptoglobin expression in rat liver. in Archives of Biological Sciences. 2020;72(4):555-565.
doi:10.2298/ABS200928049M .

Martinović, Vesna, Arambašić Jovanović, Jelena, Bogojević, Desanka, Ivanović, Anđelija, Otašević, Vesna, Stančić, Ana, Grigorov, Ilijana, "Contribution of O-GlcNAc modification of NF-κB p65 in the attenuation of diabetes-induced haptoglobin expression in rat liver" in Archives of Biological Sciences, 72, no. 4 (2020):555-565,
https://doi.org/10.2298/ABS200928049M . .

TY  - CONF
AU  - Đurašević, Siniša
AU  - Stojković, Maja
AU  - Bogdanović, Ljiljana
AU  - Grigorov, Ilijana
AU  - Bogojević, Desanka
AU  - Jasnić, Nebojša
AU  - Vujović, Predrag
AU  - Dakić, Tamara
AU  - Todorović, Zoran
AU  - Đorđević, Jelena
PY  - 2019
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6333
AB  - Acute renal ischemia/reperfusion (I/R) is a temporary restriction of kidney blood supply, followed by blood flow restoration and re-oxygenation. During I/R, decreased oxygen supply disturbs ion transport, intracellular ATP, calcium and pH levels, and numerous signalling pathways. Upon reperfusion, a restoration of oxygen level rises a reactive oxygen species generation, cytokines and chemokines release from activated tissue-resident macrophages, and infiltration of pro-inflammatory neutrophils into ischemic tissues. All these changes result in cell swelling and rupturing, and consequent necrotic or apoptotic cell death. Meldonium is an anti-ischemic drug clinically used to treat myocardial and cerebral ischemia, which acts by shifting energy production from fatty acid oxidation to glycolysis. We investigated the effects of a 4-week meldonium pre-treatment with 300 mg/kg b.m./day of rats subjected to a well-established experimental model of renal I/R, with ischemia lasting for 45 minutes, followed by 4 hours of reperfusion. The degree of apoptosis and necrosis was evaluated by measuring renal pro-apoptotic Bax and anti-apoptotic Bcl-2 ratio, serum and kidney levels of necrotic marker - high mobility group box 1 protein (HMGB1), together with the kidney histology analysis. Our results showed that apoptotic and necrotic cell death occur simultaneously under I/R conditions, judging by the renal Bax/Bcl2 ratio rise (2.7-fold), increase in serum (22%) and renal (30%) levels of HMGB1, as well as severe tubular necrosis with dilatation of the tubular structure, cast formation, tubular lumina dilatation, brush border reduction, and loss in some renal areas cells. Meldonium pretreatment reduced the elevated Bax/Bcl2 ratio by 35%, as well as the serum and renal HMGB1 levels by 20% and notably diminished histological evidence of renal I/R necrotic injury, especially regarding tubular structures. These findings proved that meldonium protects renal cells against I/R-induced necrosis and apoptosis.
PB  - Belgrade: Institute for Biological Research "Siniša Stanković"– National Institute of Republic of Serbia, University of Belgrade
C3  - Immunology at the Confluence of Multidisciplinary Approaches
T1  - Meldonium prevents acute ishemia/reperfusion inducend-renal cells death in rats
SP  - 86
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_6333
ER  - 

@conference{
author = "Đurašević, Siniša and Stojković, Maja and Bogdanović, Ljiljana and Grigorov, Ilijana and Bogojević, Desanka and Jasnić, Nebojša and Vujović, Predrag and Dakić, Tamara and Todorović, Zoran and Đorđević, Jelena",
year = "2019",
abstract = "Acute renal ischemia/reperfusion (I/R) is a temporary restriction of kidney blood supply, followed by blood flow restoration and re-oxygenation. During I/R, decreased oxygen supply disturbs ion transport, intracellular ATP, calcium and pH levels, and numerous signalling pathways. Upon reperfusion, a restoration of oxygen level rises a reactive oxygen species generation, cytokines and chemokines release from activated tissue-resident macrophages, and infiltration of pro-inflammatory neutrophils into ischemic tissues. All these changes result in cell swelling and rupturing, and consequent necrotic or apoptotic cell death. Meldonium is an anti-ischemic drug clinically used to treat myocardial and cerebral ischemia, which acts by shifting energy production from fatty acid oxidation to glycolysis. We investigated the effects of a 4-week meldonium pre-treatment with 300 mg/kg b.m./day of rats subjected to a well-established experimental model of renal I/R, with ischemia lasting for 45 minutes, followed by 4 hours of reperfusion. The degree of apoptosis and necrosis was evaluated by measuring renal pro-apoptotic Bax and anti-apoptotic Bcl-2 ratio, serum and kidney levels of necrotic marker - high mobility group box 1 protein (HMGB1), together with the kidney histology analysis. Our results showed that apoptotic and necrotic cell death occur simultaneously under I/R conditions, judging by the renal Bax/Bcl2 ratio rise (2.7-fold), increase in serum (22%) and renal (30%) levels of HMGB1, as well as severe tubular necrosis with dilatation of the tubular structure, cast formation, tubular lumina dilatation, brush border reduction, and loss in some renal areas cells. Meldonium pretreatment reduced the elevated Bax/Bcl2 ratio by 35%, as well as the serum and renal HMGB1 levels by 20% and notably diminished histological evidence of renal I/R necrotic injury, especially regarding tubular structures. These findings proved that meldonium protects renal cells against I/R-induced necrosis and apoptosis.",
publisher = "Belgrade: Institute for Biological Research "Siniša Stanković"– National Institute of Republic of Serbia, University of Belgrade",
journal = "Immunology at the Confluence of Multidisciplinary Approaches",
title = "Meldonium prevents acute ishemia/reperfusion inducend-renal cells death in rats",
pages = "86",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_6333"
}

Đurašević, S., Stojković, M., Bogdanović, L., Grigorov, I., Bogojević, D., Jasnić, N., Vujović, P., Dakić, T., Todorović, Z.,& Đorđević, J.. (2019). Meldonium prevents acute ishemia/reperfusion inducend-renal cells death in rats. in Immunology at the Confluence of Multidisciplinary Approaches
Belgrade: Institute for Biological Research "Siniša Stanković"– National Institute of Republic of Serbia, University of Belgrade., 86.
https://hdl.handle.net/21.15107/rcub_ibiss_6333

Đurašević S, Stojković M, Bogdanović L, Grigorov I, Bogojević D, Jasnić N, Vujović P, Dakić T, Todorović Z, Đorđević J. Meldonium prevents acute ishemia/reperfusion inducend-renal cells death in rats. in Immunology at the Confluence of Multidisciplinary Approaches. 2019;:86.
https://hdl.handle.net/21.15107/rcub_ibiss_6333 .

Đurašević, Siniša, Stojković, Maja, Bogdanović, Ljiljana, Grigorov, Ilijana, Bogojević, Desanka, Jasnić, Nebojša, Vujović, Predrag, Dakić, Tamara, Todorović, Zoran, Đorđević, Jelena, "Meldonium prevents acute ishemia/reperfusion inducend-renal cells death in rats" in Immunology at the Confluence of Multidisciplinary Approaches (2019):86,
https://hdl.handle.net/21.15107/rcub_ibiss_6333 .

TY  - JOUR
AU  - Đurašević, Siniša
AU  - Stojković, Maja
AU  - Bogdanović, Ljiljana
AU  - Pavlović, Slađan
AU  - Borković Mitić, Slavica
AU  - Grigorov, Ilijana
AU  - Bogojević, Desanka
AU  - Jasnić, Nebojša
AU  - Tosti, Tomislav
AU  - Đurović, Saša
AU  - Đorđević, Jelena
AU  - Todorović, Zoran
PY  - 2019
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3519
AB  - Acute renal ischemia/reperfusion (I/R) injury is a clinical condition that is challenging to
treat. Meldonium is an anti-ischemic agent that shifts energy production from fatty acid oxidation
to less oxygen-consuming glycolysis. Thus, in this study we investigated the effects of a four-week
meldonium pre-treatment (300 mg/kg b.m./day) on acute renal I/R in male rats (Wistar strain). Our
results showed that meldonium decreased animal body mass gain, food and water intake, and
carnitine, glucose, and lactic acid kidney content. In kidneys of animals subjected to I/R, meldonium
increased phosphorylation of mitogen-activated protein kinase p38 and protein kinase B, and
increased the expression of nuclear factor erythroid 2-related factor 2 and haeme oxygenase 1,
causing manganese superoxide dismutase expression and activity to increase, as well as lipid
peroxidation, cooper-zinc superoxide dismutase, glutathione peroxidase, and glutathione reductase
activities to decrease. By decreasing the kidney Bax/Bcl2 expression ratio and kidney and serum
high mobility group box 1 protein content, meldonium reduced apoptotic and necrotic events in
I/R, as confirmed by kidney histology. Meldonium increased adrenal noradrenaline content and
serum, adrenal, hepatic, and renal ascorbic/dehydroascorbic acid ratio, which caused complex
changes in renal lipidomics. Taken together, our results have confirmed that meldonium pretreatment protects against I/R-induced oxidative stress and apoptosis/necrosis.
PB  - MDPI
T2  - International Journal of Molecular Sciences
T1  - The effects of meldonium on the renal acute ischemia/reperfusion injury in rats
IS  - 22
VL  - 20
DO  - 10.3390/ijms20225747
SP  - 5747
ER  - 

@article{
author = "Đurašević, Siniša and Stojković, Maja and Bogdanović, Ljiljana and Pavlović, Slađan and Borković Mitić, Slavica and Grigorov, Ilijana and Bogojević, Desanka and Jasnić, Nebojša and Tosti, Tomislav and Đurović, Saša and Đorđević, Jelena and Todorović, Zoran",
year = "2019",
abstract = "Acute renal ischemia/reperfusion (I/R) injury is a clinical condition that is challenging to
treat. Meldonium is an anti-ischemic agent that shifts energy production from fatty acid oxidation
to less oxygen-consuming glycolysis. Thus, in this study we investigated the effects of a four-week
meldonium pre-treatment (300 mg/kg b.m./day) on acute renal I/R in male rats (Wistar strain). Our
results showed that meldonium decreased animal body mass gain, food and water intake, and
carnitine, glucose, and lactic acid kidney content. In kidneys of animals subjected to I/R, meldonium
increased phosphorylation of mitogen-activated protein kinase p38 and protein kinase B, and
increased the expression of nuclear factor erythroid 2-related factor 2 and haeme oxygenase 1,
causing manganese superoxide dismutase expression and activity to increase, as well as lipid
peroxidation, cooper-zinc superoxide dismutase, glutathione peroxidase, and glutathione reductase
activities to decrease. By decreasing the kidney Bax/Bcl2 expression ratio and kidney and serum
high mobility group box 1 protein content, meldonium reduced apoptotic and necrotic events in
I/R, as confirmed by kidney histology. Meldonium increased adrenal noradrenaline content and
serum, adrenal, hepatic, and renal ascorbic/dehydroascorbic acid ratio, which caused complex
changes in renal lipidomics. Taken together, our results have confirmed that meldonium pretreatment protects against I/R-induced oxidative stress and apoptosis/necrosis.",
publisher = "MDPI",
journal = "International Journal of Molecular Sciences",
title = "The effects of meldonium on the renal acute ischemia/reperfusion injury in rats",
number = "22",
volume = "20",
doi = "10.3390/ijms20225747",
pages = "5747"
}

Đurašević, S., Stojković, M., Bogdanović, L., Pavlović, S., Borković Mitić, S., Grigorov, I., Bogojević, D., Jasnić, N., Tosti, T., Đurović, S., Đorđević, J.,& Todorović, Z.. (2019). The effects of meldonium on the renal acute ischemia/reperfusion injury in rats. in International Journal of Molecular Sciences
MDPI., 20(22), 5747.
https://doi.org/10.3390/ijms20225747

Đurašević S, Stojković M, Bogdanović L, Pavlović S, Borković Mitić S, Grigorov I, Bogojević D, Jasnić N, Tosti T, Đurović S, Đorđević J, Todorović Z. The effects of meldonium on the renal acute ischemia/reperfusion injury in rats. in International Journal of Molecular Sciences. 2019;20(22):5747.
doi:10.3390/ijms20225747 .

Đurašević, Siniša, Stojković, Maja, Bogdanović, Ljiljana, Pavlović, Slađan, Borković Mitić, Slavica, Grigorov, Ilijana, Bogojević, Desanka, Jasnić, Nebojša, Tosti, Tomislav, Đurović, Saša, Đorđević, Jelena, Todorović, Zoran, "The effects of meldonium on the renal acute ischemia/reperfusion injury in rats" in International Journal of Molecular Sciences, 20, no. 22 (2019):5747,
https://doi.org/10.3390/ijms20225747 . .

TY  - CONF
AU  - Petrović, Anja
AU  - Bogojević, Desanka
AU  - Ivanović-Matić, Svetlana
AU  - Martinović, Vesna
AU  - Korać, Aleksandra
AU  - Jovanović-Stojanov, Sofija
AU  - Grigorov, Ilijana
PY  - 2018
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5660
AB  - Oxidative stress. cell damage and cell death underlies the etiology of liver damage/dysfunction  in  diabetes.  Bigh  Mobility  Group  Box 1 (HMGB1) is a nuclear protein that is  released  from damaged/stressed  liver cells during, diabetes and  contributes to oxidative  stresse-mediated autophagy  an cell death/survival. Since ethyl pyruvate (EP) an HMGB1 relase/expession and autophagy in the liver of diabetic rats. Diabetes was indused by streptozotocin(65mg/kg). Pretreated group of diabetes rats- (EP+D) startedl treatment  with EP (80mg/kg/daily) three·days before
diabetes induction,  while  in  the  second  group  (D+EP}  treatment  start   ten  days after diabetes induuction. In compcarison with D+EP group, EP+D group had better glycemic  status  and  higher  activity  of  antioxidative enzyme  SOD  and CAT in diabetic  liver.  According  to  western  immunoblot   analyses,  EP+D  group   sliowed higher     expression     of     extracellular    HMGB l     in    comparison      with D+EP. Consequently  detected increase in HMGB1/RAGE interactions in EP+D group were followed  by higher expression of LC3-II, HMGB1/Beclin 1 interaction and activation  of  autophagy.  Expression  of  LC3-II  and   HMGB1/Beclin 1 interaction were  at  the  control  level  in  D+EP.  Preserved  liver   morphology  in  both  EP   treated groups, observed  by  electron  microscopy,   implicated  existence   of   adaptive mechanisms  in EP+D  group.  Further  analyses  showed that  protective autophagy (mitophagy) was enhanced in EP+D group compared with diabetic and D+EP groups. Thus treatment of  diabetic  patients  with  EP  may  constitute  a  new strategy for the treatment  of  diabetes related  tissue  injury.
PB  - Belgrade: Serbian Physiological Society
C3  - Abstract book: 4th Congress of Physiological Sciences of Serbia with International Participation: Current Trends in Physiological Sciences: from cell signals to the biology of aging; 2018 Sep 19-23; Niš, Serbia
T1  - Pretreatment of diabetic rats with ethyl piruvate upregulates HMGB-driven protective autophagy in the liver
SP  - 108
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5660
ER  - 

@conference{
author = "Petrović, Anja and Bogojević, Desanka and Ivanović-Matić, Svetlana and Martinović, Vesna and Korać, Aleksandra and Jovanović-Stojanov, Sofija and Grigorov, Ilijana",
year = "2018",
abstract = "Oxidative stress. cell damage and cell death underlies the etiology of liver damage/dysfunction  in  diabetes.  Bigh  Mobility  Group  Box 1 (HMGB1) is a nuclear protein that is  released  from damaged/stressed  liver cells during, diabetes and  contributes to oxidative  stresse-mediated autophagy  an cell death/survival. Since ethyl pyruvate (EP) an HMGB1 relase/expession and autophagy in the liver of diabetic rats. Diabetes was indused by streptozotocin(65mg/kg). Pretreated group of diabetes rats- (EP+D) startedl treatment  with EP (80mg/kg/daily) three·days before
diabetes induction,  while  in  the  second  group  (D+EP}  treatment  start   ten  days after diabetes induuction. In compcarison with D+EP group, EP+D group had better glycemic  status  and  higher  activity  of  antioxidative enzyme  SOD  and CAT in diabetic  liver.  According  to  western  immunoblot   analyses,  EP+D  group   sliowed higher     expression     of     extracellular    HMGB l     in    comparison      with D+EP. Consequently  detected increase in HMGB1/RAGE interactions in EP+D group were followed  by higher expression of LC3-II, HMGB1/Beclin 1 interaction and activation  of  autophagy.  Expression  of  LC3-II  and   HMGB1/Beclin 1 interaction were  at  the  control  level  in  D+EP.  Preserved  liver   morphology  in  both  EP   treated groups, observed  by  electron  microscopy,   implicated  existence   of   adaptive mechanisms  in EP+D  group.  Further  analyses  showed that  protective autophagy (mitophagy) was enhanced in EP+D group compared with diabetic and D+EP groups. Thus treatment of  diabetic  patients  with  EP  may  constitute  a  new strategy for the treatment  of  diabetes related  tissue  injury.",
publisher = "Belgrade: Serbian Physiological Society",
journal = "Abstract book: 4th Congress of Physiological Sciences of Serbia with International Participation: Current Trends in Physiological Sciences: from cell signals to the biology of aging; 2018 Sep 19-23; Niš, Serbia",
title = "Pretreatment of diabetic rats with ethyl piruvate upregulates HMGB-driven protective autophagy in the liver",
pages = "108",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5660"
}

Petrović, A., Bogojević, D., Ivanović-Matić, S., Martinović, V., Korać, A., Jovanović-Stojanov, S.,& Grigorov, I.. (2018). Pretreatment of diabetic rats with ethyl piruvate upregulates HMGB-driven protective autophagy in the liver. in Abstract book: 4th Congress of Physiological Sciences of Serbia with International Participation: Current Trends in Physiological Sciences: from cell signals to the biology of aging; 2018 Sep 19-23; Niš, Serbia
Belgrade: Serbian Physiological Society., 108.
https://hdl.handle.net/21.15107/rcub_ibiss_5660

Petrović A, Bogojević D, Ivanović-Matić S, Martinović V, Korać A, Jovanović-Stojanov S, Grigorov I. Pretreatment of diabetic rats with ethyl piruvate upregulates HMGB-driven protective autophagy in the liver. in Abstract book: 4th Congress of Physiological Sciences of Serbia with International Participation: Current Trends in Physiological Sciences: from cell signals to the biology of aging; 2018 Sep 19-23; Niš, Serbia. 2018;:108.
https://hdl.handle.net/21.15107/rcub_ibiss_5660 .

Petrović, Anja, Bogojević, Desanka, Ivanović-Matić, Svetlana, Martinović, Vesna, Korać, Aleksandra, Jovanović-Stojanov, Sofija, Grigorov, Ilijana, "Pretreatment of diabetic rats with ethyl piruvate upregulates HMGB-driven protective autophagy in the liver" in Abstract book: 4th Congress of Physiological Sciences of Serbia with International Participation: Current Trends in Physiological Sciences: from cell signals to the biology of aging; 2018 Sep 19-23; Niš, Serbia (2018):108,
https://hdl.handle.net/21.15107/rcub_ibiss_5660 .

TY  - CONF
AU  - Petrović, Anja
AU  - Bogojević, Desanka
AU  - Ivanović Matić, Svetlana
AU  - Martinović, Vesna
AU  - Korać, Aleksandra
AU  - Jovanović Stojanov, Sofija
AU  - Poznanović, Goran
AU  - Grigorov, Ilijana
PY  - 2018
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5237
AB  - Oxidative stress through changes in antioxidative enzyme activities, glutathione metabolism and lipid peroxidation, leads to cell damage and even cell death. These changes are integrated in the pathogenetic mechanisms of the long-term, specific complications of diabetes, such as neuropathy, retinopathy, cardiomyopathy, nephropathy and hepatopathy. Recent studies have shed light on new redox sensitive endogenous targets which are important regulators of oxidative stress-induced damage. HMGB1 is a nuclear chaperone with an inflammatory function when released in the extracellular space. Extracellular HMGB1, through interaction with TLR4 receptors in its oxidized state, and with RAGE in its reduced state, controls the equilibrium between apoptosis and autophagy. HMGB1 is  a redox sensitive protein with a potentially harmful role. We therefore analyzed the changes in HMGB1 regulated signaling pathways by immunoprecipitation and Western blot that can lead to cell death or cell survival in the liver of streptozotocin (STZ)-induced diabetic rats during decreased oxidative stress after melatonin administration, and when HMGB1 release was inhibited by ethyl pyruvate. Inhibition of HMGB1 release decreased both apoptosis and autophagy, and supported the unchanged state in liver cells in STZ-treated rats as compared to the control animals. The decrease in oxidative stress achieved with melatonin decreased HMGB1 driven apoptosis but upregulated HMGB1 regulated protective autophagy, mitophagy in particular as the second level of antioxidative defense which was detected by electron microscopy. It provided a selective advantage, minimizing oxidant insults when primary antioxidant activities are compromised during oxidative stress. This adaptation led to improved cell survival in the liver of STZ-treated rats. These results showed that modulation of the role of HMGB1 in the extracellular space that was achieved by a decrease in oxidative stress is more desirable than complete inhibition of its release because HMGB1 has a protective role against oxidative injuries in diabetic liver.
PB  - Belgrade: Serbian Society for Mitochondrial and Free Radical Physiology
C3  - Book of Abstracts: Fourth Congress Challenges in Redox Biology: SSMFRP-2018; 2018 Sep 28-30; Belgrade, Serbia
T1  - The level of oxidative stress determines the role of extracellular HMGB1 protein in diabetic liver
SP  - 43
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5237
ER  - 

@conference{
author = "Petrović, Anja and Bogojević, Desanka and Ivanović Matić, Svetlana and Martinović, Vesna and Korać, Aleksandra and Jovanović Stojanov, Sofija and Poznanović, Goran and Grigorov, Ilijana",
year = "2018",
abstract = "Oxidative stress through changes in antioxidative enzyme activities, glutathione metabolism and lipid peroxidation, leads to cell damage and even cell death. These changes are integrated in the pathogenetic mechanisms of the long-term, specific complications of diabetes, such as neuropathy, retinopathy, cardiomyopathy, nephropathy and hepatopathy. Recent studies have shed light on new redox sensitive endogenous targets which are important regulators of oxidative stress-induced damage. HMGB1 is a nuclear chaperone with an inflammatory function when released in the extracellular space. Extracellular HMGB1, through interaction with TLR4 receptors in its oxidized state, and with RAGE in its reduced state, controls the equilibrium between apoptosis and autophagy. HMGB1 is  a redox sensitive protein with a potentially harmful role. We therefore analyzed the changes in HMGB1 regulated signaling pathways by immunoprecipitation and Western blot that can lead to cell death or cell survival in the liver of streptozotocin (STZ)-induced diabetic rats during decreased oxidative stress after melatonin administration, and when HMGB1 release was inhibited by ethyl pyruvate. Inhibition of HMGB1 release decreased both apoptosis and autophagy, and supported the unchanged state in liver cells in STZ-treated rats as compared to the control animals. The decrease in oxidative stress achieved with melatonin decreased HMGB1 driven apoptosis but upregulated HMGB1 regulated protective autophagy, mitophagy in particular as the second level of antioxidative defense which was detected by electron microscopy. It provided a selective advantage, minimizing oxidant insults when primary antioxidant activities are compromised during oxidative stress. This adaptation led to improved cell survival in the liver of STZ-treated rats. These results showed that modulation of the role of HMGB1 in the extracellular space that was achieved by a decrease in oxidative stress is more desirable than complete inhibition of its release because HMGB1 has a protective role against oxidative injuries in diabetic liver.",
publisher = "Belgrade: Serbian Society for Mitochondrial and Free Radical Physiology",
journal = "Book of Abstracts: Fourth Congress Challenges in Redox Biology: SSMFRP-2018; 2018 Sep 28-30; Belgrade, Serbia",
title = "The level of oxidative stress determines the role of extracellular HMGB1 protein in diabetic liver",
pages = "43",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5237"
}

Petrović, A., Bogojević, D., Ivanović Matić, S., Martinović, V., Korać, A., Jovanović Stojanov, S., Poznanović, G.,& Grigorov, I.. (2018). The level of oxidative stress determines the role of extracellular HMGB1 protein in diabetic liver. in Book of Abstracts: Fourth Congress Challenges in Redox Biology: SSMFRP-2018; 2018 Sep 28-30; Belgrade, Serbia
Belgrade: Serbian Society for Mitochondrial and Free Radical Physiology., 43.
https://hdl.handle.net/21.15107/rcub_ibiss_5237

Petrović A, Bogojević D, Ivanović Matić S, Martinović V, Korać A, Jovanović Stojanov S, Poznanović G, Grigorov I. The level of oxidative stress determines the role of extracellular HMGB1 protein in diabetic liver. in Book of Abstracts: Fourth Congress Challenges in Redox Biology: SSMFRP-2018; 2018 Sep 28-30; Belgrade, Serbia. 2018;:43.
https://hdl.handle.net/21.15107/rcub_ibiss_5237 .

Petrović, Anja, Bogojević, Desanka, Ivanović Matić, Svetlana, Martinović, Vesna, Korać, Aleksandra, Jovanović Stojanov, Sofija, Poznanović, Goran, Grigorov, Ilijana, "The level of oxidative stress determines the role of extracellular HMGB1 protein in diabetic liver" in Book of Abstracts: Fourth Congress Challenges in Redox Biology: SSMFRP-2018; 2018 Sep 28-30; Belgrade, Serbia (2018):43,
https://hdl.handle.net/21.15107/rcub_ibiss_5237 .

TY  - JOUR
AU  - Jovanović Stojanov, Sofija
AU  - Martinović, Vesna
AU  - Bogojević, Desanka
AU  - Poznanović, Goran
AU  - Petrović, Anja
AU  - Ivanović Matić, Svetlana
AU  - Grigorov, Ilijana
PY  - 2018
UR  - http://link.springer.com/10.1007/s13105-018-0626-0
UR  - http://www.ncbi.nlm.nih.gov/pubmed/29611132
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3068
AB  - Chronic inflammation plays an essential role in the development of diabetic complications. Understanding the molecular mechanisms that support inflammation is a prerequisite for the design of novel anti-inflammatory therapies. These would take into consideration circulating levels of cytokines and damage-associated molecular patterns (DAMPs) that include the high mobility group box 1 (HMGB1) protein which, in part, promotes the inflammatory response through TLR4 signaling. The liver, as the source of circulating cytokines and acute-phase proteins, contributes to the control of systemic inflammation. We previously found that liver injury in streptozotocin-induced diabetic rats correlated with the level of oxidative stress, increased expression of HMGB1, and with the activation of TLR4-mediated cell death pathways. In the present work, we examined the effects of ethyl pyruvate (EP), an inhibitor of HMGB1 release/expression, on the modulation of activation of the HMGB1/TLR4 inflammatory cascade in diabetic liver. We observed that increased expression of inflammatory markers, TNF-α, IL-6, and haptoglobin in diabetic liver was associated with increased HMGB1/TLR4 interaction, activation of MAPK (p38, ERK, JNK)/NF-κB p65 and JAK1/STAT3 signaling pathways, and with decreased expression of Nrf2-regulated antioxidative enzymes. The reduction in HMGB1 expression as the result of EP administration reduced the pro-inflammatory activity of HMGB1 and exerted a protective effect on diabetic liver, which was observed as improved liver histology and antioxidant and inflammatory statuses. Our results suggest that prevention of HMGB1 release and blockage of the HMGB/TLR4 axis represents a potentially effective therapeutic strategy aimed at ameliorating diabetes-induced inflammation and ensuing liver injury.
T2  - Journal of Physiology and Biochemistry
T1  - Modulation of diabetes-related liver injury by the HMGB1/TLR4 inflammatory pathway.
IS  - 2
VL  - 74
DO  - 10.1007/s13105-018-0626-0
SP  - 345
EP  - 358
ER  - 

@article{
author = "Jovanović Stojanov, Sofija and Martinović, Vesna and Bogojević, Desanka and Poznanović, Goran and Petrović, Anja and Ivanović Matić, Svetlana and Grigorov, Ilijana",
year = "2018",
abstract = "Chronic inflammation plays an essential role in the development of diabetic complications. Understanding the molecular mechanisms that support inflammation is a prerequisite for the design of novel anti-inflammatory therapies. These would take into consideration circulating levels of cytokines and damage-associated molecular patterns (DAMPs) that include the high mobility group box 1 (HMGB1) protein which, in part, promotes the inflammatory response through TLR4 signaling. The liver, as the source of circulating cytokines and acute-phase proteins, contributes to the control of systemic inflammation. We previously found that liver injury in streptozotocin-induced diabetic rats correlated with the level of oxidative stress, increased expression of HMGB1, and with the activation of TLR4-mediated cell death pathways. In the present work, we examined the effects of ethyl pyruvate (EP), an inhibitor of HMGB1 release/expression, on the modulation of activation of the HMGB1/TLR4 inflammatory cascade in diabetic liver. We observed that increased expression of inflammatory markers, TNF-α, IL-6, and haptoglobin in diabetic liver was associated with increased HMGB1/TLR4 interaction, activation of MAPK (p38, ERK, JNK)/NF-κB p65 and JAK1/STAT3 signaling pathways, and with decreased expression of Nrf2-regulated antioxidative enzymes. The reduction in HMGB1 expression as the result of EP administration reduced the pro-inflammatory activity of HMGB1 and exerted a protective effect on diabetic liver, which was observed as improved liver histology and antioxidant and inflammatory statuses. Our results suggest that prevention of HMGB1 release and blockage of the HMGB/TLR4 axis represents a potentially effective therapeutic strategy aimed at ameliorating diabetes-induced inflammation and ensuing liver injury.",
journal = "Journal of Physiology and Biochemistry",
title = "Modulation of diabetes-related liver injury by the HMGB1/TLR4 inflammatory pathway.",
number = "2",
volume = "74",
doi = "10.1007/s13105-018-0626-0",
pages = "345-358"
}

Jovanović Stojanov, S., Martinović, V., Bogojević, D., Poznanović, G., Petrović, A., Ivanović Matić, S.,& Grigorov, I.. (2018). Modulation of diabetes-related liver injury by the HMGB1/TLR4 inflammatory pathway.. in Journal of Physiology and Biochemistry, 74(2), 345-358.
https://doi.org/10.1007/s13105-018-0626-0

Jovanović Stojanov S, Martinović V, Bogojević D, Poznanović G, Petrović A, Ivanović Matić S, Grigorov I. Modulation of diabetes-related liver injury by the HMGB1/TLR4 inflammatory pathway.. in Journal of Physiology and Biochemistry. 2018;74(2):345-358.
doi:10.1007/s13105-018-0626-0 .

Jovanović Stojanov, Sofija, Martinović, Vesna, Bogojević, Desanka, Poznanović, Goran, Petrović, Anja, Ivanović Matić, Svetlana, Grigorov, Ilijana, "Modulation of diabetes-related liver injury by the HMGB1/TLR4 inflammatory pathway." in Journal of Physiology and Biochemistry, 74, no. 2 (2018):345-358,
https://doi.org/10.1007/s13105-018-0626-0 . .

TY  - CONF
AU  - Jovanović Stojanov, Sofija
AU  - Grigorov, Ilijana
AU  - Petrović, Anja
AU  - Bogojević, Desanka
AU  - Ivanović Matić, Svetlana
AU  - Martinović, Vesna
PY  - 2017
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5246
AB  - Introduction: Oxidative stress and chronic low-grade inflammation in diabetes leads to liver injury. During diabetes, extracellular level of high-mobility group box-1 (HMGB1) protein increases. Considering that extracellular HMGB1 (eHMGB1) protein functions as an pro-inflammatory mediator, triggering inflammatory responses by promoting the expression of inflammatory cytokines, the aim of this study was to investigate its contribution to the maintenance of inflammatory condition in the liver of diabetic rats. This may help to better understand diabetes-induced liver pathologies and potentially provide target to develop efficient therapies. Methods: Diabetes was induced by a single intraperitoneal (ip) injection of STZ (65 mg/kg). Inflammatory status in the rat liver was determined in the fourth week after diabetes induction by measuring expression of pro-inflammatory cytokines (TNFα, IL- 6) and related production of anti-inflammatory protein haptoglobin (Hp). We also studied the effects of HMGB1 on inflammation through its interaction with TLR4 and related downstream signaling pathways in terms of inhibited HMGB1 secretion in diabetic rats by ethyl pyruvate (EP) treatment (80 mg/kg/ip/daily). Results: The results show that decrease in eHMGB1 expression caused by EP treatment, correlates with reduced level of TNFα, IL-6 and Hp in the serum and liver of diabetic rats. These changes are in accordance with significant decrease in HMGB1/TLR4 interaction and decreased activation of MAPK (p38, ERK, JNK), NF-κB p65 and JAK1/STAT3 signaling pathways in diabetic liver. Conclusion: In diabetic liver eHMGB1 is involved in the inflammatory response dually. It acts pro-inflammatory by enhancing production of inflammatory mediators and anti-inflammatory by increasing Hp expression.
PB  - Belgrade: University of Belgrade, Faculty of Biology
C3  - Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.
T1  - Pro-inflamatory and anti-inflamatory role of HMGB1 in the liver of diabetic rats
SP  - 44
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5246
ER  - 

@conference{
author = "Jovanović Stojanov, Sofija and Grigorov, Ilijana and Petrović, Anja and Bogojević, Desanka and Ivanović Matić, Svetlana and Martinović, Vesna",
year = "2017",
abstract = "Introduction: Oxidative stress and chronic low-grade inflammation in diabetes leads to liver injury. During diabetes, extracellular level of high-mobility group box-1 (HMGB1) protein increases. Considering that extracellular HMGB1 (eHMGB1) protein functions as an pro-inflammatory mediator, triggering inflammatory responses by promoting the expression of inflammatory cytokines, the aim of this study was to investigate its contribution to the maintenance of inflammatory condition in the liver of diabetic rats. This may help to better understand diabetes-induced liver pathologies and potentially provide target to develop efficient therapies. Methods: Diabetes was induced by a single intraperitoneal (ip) injection of STZ (65 mg/kg). Inflammatory status in the rat liver was determined in the fourth week after diabetes induction by measuring expression of pro-inflammatory cytokines (TNFα, IL- 6) and related production of anti-inflammatory protein haptoglobin (Hp). We also studied the effects of HMGB1 on inflammation through its interaction with TLR4 and related downstream signaling pathways in terms of inhibited HMGB1 secretion in diabetic rats by ethyl pyruvate (EP) treatment (80 mg/kg/ip/daily). Results: The results show that decrease in eHMGB1 expression caused by EP treatment, correlates with reduced level of TNFα, IL-6 and Hp in the serum and liver of diabetic rats. These changes are in accordance with significant decrease in HMGB1/TLR4 interaction and decreased activation of MAPK (p38, ERK, JNK), NF-κB p65 and JAK1/STAT3 signaling pathways in diabetic liver. Conclusion: In diabetic liver eHMGB1 is involved in the inflammatory response dually. It acts pro-inflammatory by enhancing production of inflammatory mediators and anti-inflammatory by increasing Hp expression.",
publisher = "Belgrade: University of Belgrade, Faculty of Biology",
journal = "Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.",
title = "Pro-inflamatory and anti-inflamatory role of HMGB1 in the liver of diabetic rats",
pages = "44",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5246"
}

Jovanović Stojanov, S., Grigorov, I., Petrović, A., Bogojević, D., Ivanović Matić, S.,& Martinović, V.. (2017). Pro-inflamatory and anti-inflamatory role of HMGB1 in the liver of diabetic rats. in Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.
Belgrade: University of Belgrade, Faculty of Biology., 44.
https://hdl.handle.net/21.15107/rcub_ibiss_5246

Jovanović Stojanov S, Grigorov I, Petrović A, Bogojević D, Ivanović Matić S, Martinović V. Pro-inflamatory and anti-inflamatory role of HMGB1 in the liver of diabetic rats. in Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.. 2017;:44.
https://hdl.handle.net/21.15107/rcub_ibiss_5246 .

Jovanović Stojanov, Sofija, Grigorov, Ilijana, Petrović, Anja, Bogojević, Desanka, Ivanović Matić, Svetlana, Martinović, Vesna, "Pro-inflamatory and anti-inflamatory role of HMGB1 in the liver of diabetic rats" in Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia. (2017):44,
https://hdl.handle.net/21.15107/rcub_ibiss_5246 .

TY  - CONF
AU  - Petrović, Anja
AU  - Ivanović Matić, Svetlana
AU  - Bogojević, Desanka
AU  - Martinović, Vesna
AU  - Korać, Aleksandra
AU  - Jovanović Stojanov, Sofija
AU  - Stevanović, Jelena
AU  - Grigorov, Ilijana
PY  - 2017
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5244
AB  - Introduction: Hepatocellular death is the main trigger of liver disease. Since diabetic patients are very prone to liver diseases there is a urgent need to identify key regulators of cell death processes. High-mobility group box protein 1 (HMGB1) is a non-histone nuclear protein with a role in apoptotic and autophagic activation when it is present in cytosol and extracellular space. The aim of this study was to elucidate HMGB1 contribution to liver injury trough activation of apoptosis and autophagy in streptozotocin (STZ)-induced diabetic rats since the role of HMGB1 in hepatic cell death during diabetes is partially known. Methods: Diabetes was induced with a single intraperitoneal (i.p.) injection of STZ (65 mg/kg). Inhibition of HMGB1 release was achieved by ethyl pyruvate (80 mg/kg/i.p./daily). We followed changes in expression of serum and cytosolic HMGB1 and its interaction with TLR4 and RAGE and how these changes affect on apoptotic and autophagic activity and liver morphology. Results: In the serum of diabetic rats elevated levels of HMGB1 were accompanied by increased HMGB1 interactions with TLR4 and RAGE receptors. Enhancement in these interactions led to increased activity of both apoptotic and autophagic signaling pathways resulting in altered liver morphology and acummulation of autophagosomes in hepatocytes. Inhibition of HMGB1 release caused reduction in apoptotic and autophagic activity which resulted in preservation of normal liver architecture and decreased number of autophagosomes. Conclusion: HMGB1 causes liver damage through activation of apoptosis and autophagy, therefore it’s a suitable new target for prevention of liver diseases in diabetic patients.
PB  - Belgrade: University of Belgrade, Faculty of Biology
C3  - Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.
T1  - Inhibition of HMGB1 release decreases both apoptopic and autophagic activity in the hepatocytes and reduce liver injury in streptozotocin treated rats
SP  - 65
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5244
ER  - 

@conference{
author = "Petrović, Anja and Ivanović Matić, Svetlana and Bogojević, Desanka and Martinović, Vesna and Korać, Aleksandra and Jovanović Stojanov, Sofija and Stevanović, Jelena and Grigorov, Ilijana",
year = "2017",
abstract = "Introduction: Hepatocellular death is the main trigger of liver disease. Since diabetic patients are very prone to liver diseases there is a urgent need to identify key regulators of cell death processes. High-mobility group box protein 1 (HMGB1) is a non-histone nuclear protein with a role in apoptotic and autophagic activation when it is present in cytosol and extracellular space. The aim of this study was to elucidate HMGB1 contribution to liver injury trough activation of apoptosis and autophagy in streptozotocin (STZ)-induced diabetic rats since the role of HMGB1 in hepatic cell death during diabetes is partially known. Methods: Diabetes was induced with a single intraperitoneal (i.p.) injection of STZ (65 mg/kg). Inhibition of HMGB1 release was achieved by ethyl pyruvate (80 mg/kg/i.p./daily). We followed changes in expression of serum and cytosolic HMGB1 and its interaction with TLR4 and RAGE and how these changes affect on apoptotic and autophagic activity and liver morphology. Results: In the serum of diabetic rats elevated levels of HMGB1 were accompanied by increased HMGB1 interactions with TLR4 and RAGE receptors. Enhancement in these interactions led to increased activity of both apoptotic and autophagic signaling pathways resulting in altered liver morphology and acummulation of autophagosomes in hepatocytes. Inhibition of HMGB1 release caused reduction in apoptotic and autophagic activity which resulted in preservation of normal liver architecture and decreased number of autophagosomes. Conclusion: HMGB1 causes liver damage through activation of apoptosis and autophagy, therefore it’s a suitable new target for prevention of liver diseases in diabetic patients.",
publisher = "Belgrade: University of Belgrade, Faculty of Biology",
journal = "Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.",
title = "Inhibition of HMGB1 release decreases both apoptopic and autophagic activity in the hepatocytes and reduce liver injury in streptozotocin treated rats",
pages = "65",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5244"
}

Petrović, A., Ivanović Matić, S., Bogojević, D., Martinović, V., Korać, A., Jovanović Stojanov, S., Stevanović, J.,& Grigorov, I.. (2017). Inhibition of HMGB1 release decreases both apoptopic and autophagic activity in the hepatocytes and reduce liver injury in streptozotocin treated rats. in Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.
Belgrade: University of Belgrade, Faculty of Biology., 65.
https://hdl.handle.net/21.15107/rcub_ibiss_5244

Petrović A, Ivanović Matić S, Bogojević D, Martinović V, Korać A, Jovanović Stojanov S, Stevanović J, Grigorov I. Inhibition of HMGB1 release decreases both apoptopic and autophagic activity in the hepatocytes and reduce liver injury in streptozotocin treated rats. in Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.. 2017;:65.
https://hdl.handle.net/21.15107/rcub_ibiss_5244 .

Petrović, Anja, Ivanović Matić, Svetlana, Bogojević, Desanka, Martinović, Vesna, Korać, Aleksandra, Jovanović Stojanov, Sofija, Stevanović, Jelena, Grigorov, Ilijana, "Inhibition of HMGB1 release decreases both apoptopic and autophagic activity in the hepatocytes and reduce liver injury in streptozotocin treated rats" in Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia. (2017):65,
https://hdl.handle.net/21.15107/rcub_ibiss_5244 .

TY  - CONF
AU  - Martinović, Vesna
AU  - Jovanović Stojanov, Sofija
AU  - Bogojević, Desanka
AU  - Ivanović Matić, Svetlana
AU  - Petrović, Anja
AU  - Poznanović, Goran
AU  - Grigorov, Ilijana
PY  - 2017
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5245
AB  - Introduction: Oxidative stress and inflammation are involved in the pathogenesis of diabetes. Previously, we showed that melatonin exerts potent anti-oxidative and anti-inflammatory actions in the liver of streptozotocin (STZ)-induced diabetic rats, thus correcting diabetes-associated abnormalities. The concept of a liver-spleen axis has been proposed as an intersection linking immunity and metabolism in various conditions, including chronic liver diseases. We therefore compared the effect of melatonin on oxidative stress and the inflammatory response in the liver and spleen of STZ-induced diabetic rats. Methods: Male Wistar rats were injected with 65 mg/kg STZ to induce diabetes. Melatonin was administrated daily (0.2 mg/kg/i.p) until the end of the study at 4 weeks after diabetes induction. Oxidative stress was assessed by measuring the level of lipid peroxidation and the changes in antioxidative enzyme activities. Inflammation was evaluated by examining the levels of proinflammatory cytokines, inflammatory mediators and the acute-phase protein haptoglobin (Hp). Results: In both tissues, melatonin lowered oxidative stress, which was observed as a decrease in lipid peroxidation and increased expression and activity of CAT, MnSOD and CuZnSOD. By suppressing the activation of NF-κB p65 and MAPK (p38, JNK, ERK) signaling cascades and by decreasing the production of TNF-α, IL-6, HMGB1 and Hp, melatonin also reduced inflammation. Conclusion: Melatonin stimulated the antioxidative defense in both, the spleen and liver of diabetic rats and attenuated inflammation via the same molecular mechanisms.
PB  - Belgrade: University of Belgrade, Faculty of Biology
C3  - Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.
T1  - Effect of melatonin on oxdative and inflammatory stress in spleen and liver of streptozotocin -induced diabetic rats
SP  - 55
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5245
ER  - 

@conference{
author = "Martinović, Vesna and Jovanović Stojanov, Sofija and Bogojević, Desanka and Ivanović Matić, Svetlana and Petrović, Anja and Poznanović, Goran and Grigorov, Ilijana",
year = "2017",
abstract = "Introduction: Oxidative stress and inflammation are involved in the pathogenesis of diabetes. Previously, we showed that melatonin exerts potent anti-oxidative and anti-inflammatory actions in the liver of streptozotocin (STZ)-induced diabetic rats, thus correcting diabetes-associated abnormalities. The concept of a liver-spleen axis has been proposed as an intersection linking immunity and metabolism in various conditions, including chronic liver diseases. We therefore compared the effect of melatonin on oxidative stress and the inflammatory response in the liver and spleen of STZ-induced diabetic rats. Methods: Male Wistar rats were injected with 65 mg/kg STZ to induce diabetes. Melatonin was administrated daily (0.2 mg/kg/i.p) until the end of the study at 4 weeks after diabetes induction. Oxidative stress was assessed by measuring the level of lipid peroxidation and the changes in antioxidative enzyme activities. Inflammation was evaluated by examining the levels of proinflammatory cytokines, inflammatory mediators and the acute-phase protein haptoglobin (Hp). Results: In both tissues, melatonin lowered oxidative stress, which was observed as a decrease in lipid peroxidation and increased expression and activity of CAT, MnSOD and CuZnSOD. By suppressing the activation of NF-κB p65 and MAPK (p38, JNK, ERK) signaling cascades and by decreasing the production of TNF-α, IL-6, HMGB1 and Hp, melatonin also reduced inflammation. Conclusion: Melatonin stimulated the antioxidative defense in both, the spleen and liver of diabetic rats and attenuated inflammation via the same molecular mechanisms.",
publisher = "Belgrade: University of Belgrade, Faculty of Biology",
journal = "Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.",
title = "Effect of melatonin on oxdative and inflammatory stress in spleen and liver of streptozotocin -induced diabetic rats",
pages = "55",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5245"
}

Martinović, V., Jovanović Stojanov, S., Bogojević, D., Ivanović Matić, S., Petrović, A., Poznanović, G.,& Grigorov, I.. (2017). Effect of melatonin on oxdative and inflammatory stress in spleen and liver of streptozotocin -induced diabetic rats. in Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.
Belgrade: University of Belgrade, Faculty of Biology., 55.
https://hdl.handle.net/21.15107/rcub_ibiss_5245

Martinović V, Jovanović Stojanov S, Bogojević D, Ivanović Matić S, Petrović A, Poznanović G, Grigorov I. Effect of melatonin on oxdative and inflammatory stress in spleen and liver of streptozotocin -induced diabetic rats. in Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.. 2017;:55.
https://hdl.handle.net/21.15107/rcub_ibiss_5245 .

Martinović, Vesna, Jovanović Stojanov, Sofija, Bogojević, Desanka, Ivanović Matić, Svetlana, Petrović, Anja, Poznanović, Goran, Grigorov, Ilijana, "Effect of melatonin on oxdative and inflammatory stress in spleen and liver of streptozotocin -induced diabetic rats" in Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia. (2017):55,
https://hdl.handle.net/21.15107/rcub_ibiss_5245 .

TY  - JOUR
AU  - Petrović, Anja
AU  - Bogojević, Desanka
AU  - Korać, Aleksandra
AU  - Golić, Igor
AU  - Jovanović Stojanov, Sofija
AU  - Martinović, Vesna
AU  - Ivanović Matić, Svetlana
AU  - Stevanović, Jelena
AU  - Poznanović, Goran
AU  - Grigorov, Ilijana
PY  - 2017
UR  - http://link.springer.com/10.1007/s13105-017-0574-0
UR  - http://www.ncbi.nlm.nih.gov/pubmed/28695466
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2787
AB  - The progression of oxidative stress, resulting cell damage, and cell death underlies the etiology of liver damage/dysfunction as a complication of diabetes. High-mobility group box 1 (HMGB1) protein, a chromatin-binding nuclear protein and damage-associated molecular pattern molecule, is integral to oxidative stress and signaling pathways regulating cell death and cell survival. We previously found that in streptozotocin (STZ)-induced diabetic rats, reduction of oxidative stress after melatonin administration lowered necrotic cell death and increased expression of HMGB1 and hepatocellular damage. In the present study, we examined whether alleviation of diabetes-attendant oxidative stress and ensuing change in HMGB1 expression influence the dynamic equilibrium between apoptosis/autophagy and liver damage. We observed that elevated HMGB1 protein levels in diabetic rat liver accompanied increased interactions of HMGB1 with TLR4 and RAGE, and activation of the intrinsic apoptotic pathway and Beclin 1-dependent autophagy. The absence of p62 degradation in diabetic rat liver pointed to defective autophagy which was responsible for lower autophagosome/autophagolysosome formation and an increased apoptosis/autophagy ratio. Compared to diabetic rats, in melatonin-treated diabetic rats, the structure of liver cells was preserved, HMGB1/TLR4 interaction and downstream apoptotic signaling were significantly reduced, HMGB1/Beclin 1 colocalization and interactions were augmented and Beclin 1-mediated autophagy, mithophagy in particular, were increased. We concluded that in mild oxidative stress, HMGB1 is cytoprotective, whereas in intense oxidative stress, HMGB1 actions promote cell death and liver damage. Since reduced HMGB1 binds to RAGE but not to TLR4, redox modification of HMGB1 as a mechanism regulating the cross-talk between apoptosis and autophagy in diabetes is discussed.
T2  - Journal of Physiology and Biochemistry
T1  - Oxidative stress-dependent contribution of HMGB1 to the interplay between apoptosis and autophagy in diabetic rat liver.
DO  - 10.1007/s13105-017-0574-0
ER  - 

@article{
author = "Petrović, Anja and Bogojević, Desanka and Korać, Aleksandra and Golić, Igor and Jovanović Stojanov, Sofija and Martinović, Vesna and Ivanović Matić, Svetlana and Stevanović, Jelena and Poznanović, Goran and Grigorov, Ilijana",
year = "2017",
abstract = "The progression of oxidative stress, resulting cell damage, and cell death underlies the etiology of liver damage/dysfunction as a complication of diabetes. High-mobility group box 1 (HMGB1) protein, a chromatin-binding nuclear protein and damage-associated molecular pattern molecule, is integral to oxidative stress and signaling pathways regulating cell death and cell survival. We previously found that in streptozotocin (STZ)-induced diabetic rats, reduction of oxidative stress after melatonin administration lowered necrotic cell death and increased expression of HMGB1 and hepatocellular damage. In the present study, we examined whether alleviation of diabetes-attendant oxidative stress and ensuing change in HMGB1 expression influence the dynamic equilibrium between apoptosis/autophagy and liver damage. We observed that elevated HMGB1 protein levels in diabetic rat liver accompanied increased interactions of HMGB1 with TLR4 and RAGE, and activation of the intrinsic apoptotic pathway and Beclin 1-dependent autophagy. The absence of p62 degradation in diabetic rat liver pointed to defective autophagy which was responsible for lower autophagosome/autophagolysosome formation and an increased apoptosis/autophagy ratio. Compared to diabetic rats, in melatonin-treated diabetic rats, the structure of liver cells was preserved, HMGB1/TLR4 interaction and downstream apoptotic signaling were significantly reduced, HMGB1/Beclin 1 colocalization and interactions were augmented and Beclin 1-mediated autophagy, mithophagy in particular, were increased. We concluded that in mild oxidative stress, HMGB1 is cytoprotective, whereas in intense oxidative stress, HMGB1 actions promote cell death and liver damage. Since reduced HMGB1 binds to RAGE but not to TLR4, redox modification of HMGB1 as a mechanism regulating the cross-talk between apoptosis and autophagy in diabetes is discussed.",
journal = "Journal of Physiology and Biochemistry",
title = "Oxidative stress-dependent contribution of HMGB1 to the interplay between apoptosis and autophagy in diabetic rat liver.",
doi = "10.1007/s13105-017-0574-0"
}

Petrović, A., Bogojević, D., Korać, A., Golić, I., Jovanović Stojanov, S., Martinović, V., Ivanović Matić, S., Stevanović, J., Poznanović, G.,& Grigorov, I.. (2017). Oxidative stress-dependent contribution of HMGB1 to the interplay between apoptosis and autophagy in diabetic rat liver.. in Journal of Physiology and Biochemistry.
https://doi.org/10.1007/s13105-017-0574-0

Petrović A, Bogojević D, Korać A, Golić I, Jovanović Stojanov S, Martinović V, Ivanović Matić S, Stevanović J, Poznanović G, Grigorov I. Oxidative stress-dependent contribution of HMGB1 to the interplay between apoptosis and autophagy in diabetic rat liver.. in Journal of Physiology and Biochemistry. 2017;.
doi:10.1007/s13105-017-0574-0 .

Petrović, Anja, Bogojević, Desanka, Korać, Aleksandra, Golić, Igor, Jovanović Stojanov, Sofija, Martinović, Vesna, Ivanović Matić, Svetlana, Stevanović, Jelena, Poznanović, Goran, Grigorov, Ilijana, "Oxidative stress-dependent contribution of HMGB1 to the interplay between apoptosis and autophagy in diabetic rat liver." in Journal of Physiology and Biochemistry (2017),
https://doi.org/10.1007/s13105-017-0574-0 . .

TY  - CONF
AU  - Đurašević, Siniša
AU  - Jasnić, Nebojša
AU  - Dakić, Tamara
AU  - Jevđović, Tanja
AU  - Lakić, Iva
AU  - Vujović, Predrag
AU  - Đorđević, Jelena
AU  - Mitić-Ćulafić, Dragana
AU  - Nikolić, Biljana
AU  - Grigorov, Ilijana
AU  - Bogojević, Desanka
AU  - Pavlović, Slađan
AU  - Prokić, Marko
AU  - Zaletel, Ivan
AU  - Todorović, Zoran
PY  - 2017
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3423
AB  - We investigated the effect of long-term high-dose virgin coconut oil (VCO) supplementation on rat liver and serum lipid status. Animals were divided into two groups with 8 of them in each: normally fed (Control group) and the group fed with coconut oil at a concentration of 20% in food (VCO group). The experiment lasted for four months. On the last day of the experiment animals were killed, and blood and liver tissue were collected. In serum we measured the levels of total cholesterol (TC), high-density lipoproteins (HDL), non-HDL lipoproteins, triglycerides (TG), aspartate aminotransferase (9\.ST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP). We also measured both liver and serum levels of high mobility group protein B 1 (HMGB 1) and haptoglobin (HP), as ,.vell as the liver level of NF-KB p65/ p-NF-KB p65 transcription factor, together with the histopathology analysis on liver slices and liver Comet assay. The results show that coconut oil do not change serum TC and HDL, but reduces non-HDL and TG levels (10% and 50%, respectively) comparing to control. As a result, atherogenic index of serum (AI) is strongly reduced in VCO group versus control. As for the liver status, results show that coconut supplementation increases AST, ALT and ALP levels in VCO group (50%, 30% and 60%, respectively) comparing to control. This effect is caused by the accumulation of coconut oil fat in liver, as confirmed by the histopathology showing signs of mild nonalcoholic steatohepatitis in VCO group, followed with the increased %of DNA in comet tail. The liver inflammation in VCO group is further demonstrated with the liver HP, HMGBl and p-NF-KB p65 level increase, and increase in nuclear level ofNF­kB p65, but not accompanying serum HP and HMGBl increase. In conclusion, our results show that coconut oil supplementation, despite causing mild and localized steatohepatitis, also lowers serum atherogcnic index, a predictor of cardiovascular risk.
PB  - BIT Congress Inc. (BIT Group Global Ltd.)
C3  - BIT´s 6th Annual World Congress of Food and Nutrition: Abstract Book. Shenyang, China; September 15-17, 2017
T1  - The effect of long-term high-dose coconut oil supplementation on rat sliver and serum lipids
SP  - 168
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_3423
ER  - 

@conference{
author = "Đurašević, Siniša and Jasnić, Nebojša and Dakić, Tamara and Jevđović, Tanja and Lakić, Iva and Vujović, Predrag and Đorđević, Jelena and Mitić-Ćulafić, Dragana and Nikolić, Biljana and Grigorov, Ilijana and Bogojević, Desanka and Pavlović, Slađan and Prokić, Marko and Zaletel, Ivan and Todorović, Zoran",
year = "2017",
abstract = "We investigated the effect of long-term high-dose virgin coconut oil (VCO) supplementation on rat liver and serum lipid status. Animals were divided into two groups with 8 of them in each: normally fed (Control group) and the group fed with coconut oil at a concentration of 20% in food (VCO group). The experiment lasted for four months. On the last day of the experiment animals were killed, and blood and liver tissue were collected. In serum we measured the levels of total cholesterol (TC), high-density lipoproteins (HDL), non-HDL lipoproteins, triglycerides (TG), aspartate aminotransferase (9\.ST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP). We also measured both liver and serum levels of high mobility group protein B 1 (HMGB 1) and haptoglobin (HP), as ,.vell as the liver level of NF-KB p65/ p-NF-KB p65 transcription factor, together with the histopathology analysis on liver slices and liver Comet assay. The results show that coconut oil do not change serum TC and HDL, but reduces non-HDL and TG levels (10% and 50%, respectively) comparing to control. As a result, atherogenic index of serum (AI) is strongly reduced in VCO group versus control. As for the liver status, results show that coconut supplementation increases AST, ALT and ALP levels in VCO group (50%, 30% and 60%, respectively) comparing to control. This effect is caused by the accumulation of coconut oil fat in liver, as confirmed by the histopathology showing signs of mild nonalcoholic steatohepatitis in VCO group, followed with the increased %of DNA in comet tail. The liver inflammation in VCO group is further demonstrated with the liver HP, HMGBl and p-NF-KB p65 level increase, and increase in nuclear level ofNF­kB p65, but not accompanying serum HP and HMGBl increase. In conclusion, our results show that coconut oil supplementation, despite causing mild and localized steatohepatitis, also lowers serum atherogcnic index, a predictor of cardiovascular risk.",
publisher = "BIT Congress Inc. (BIT Group Global Ltd.)",
journal = "BIT´s 6th Annual World Congress of Food and Nutrition: Abstract Book. Shenyang, China; September 15-17, 2017",
title = "The effect of long-term high-dose coconut oil supplementation on rat sliver and serum lipids",
pages = "168",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_3423"
}

Đurašević, S., Jasnić, N., Dakić, T., Jevđović, T., Lakić, I., Vujović, P., Đorđević, J., Mitić-Ćulafić, D., Nikolić, B., Grigorov, I., Bogojević, D., Pavlović, S., Prokić, M., Zaletel, I.,& Todorović, Z.. (2017). The effect of long-term high-dose coconut oil supplementation on rat sliver and serum lipids. in BIT´s 6th Annual World Congress of Food and Nutrition: Abstract Book. Shenyang, China; September 15-17, 2017
BIT Congress Inc. (BIT Group Global Ltd.)., 168.
https://hdl.handle.net/21.15107/rcub_ibiss_3423

Đurašević S, Jasnić N, Dakić T, Jevđović T, Lakić I, Vujović P, Đorđević J, Mitić-Ćulafić D, Nikolić B, Grigorov I, Bogojević D, Pavlović S, Prokić M, Zaletel I, Todorović Z. The effect of long-term high-dose coconut oil supplementation on rat sliver and serum lipids. in BIT´s 6th Annual World Congress of Food and Nutrition: Abstract Book. Shenyang, China; September 15-17, 2017. 2017;:168.
https://hdl.handle.net/21.15107/rcub_ibiss_3423 .

Đurašević, Siniša, Jasnić, Nebojša, Dakić, Tamara, Jevđović, Tanja, Lakić, Iva, Vujović, Predrag, Đorđević, Jelena, Mitić-Ćulafić, Dragana, Nikolić, Biljana, Grigorov, Ilijana, Bogojević, Desanka, Pavlović, Slađan, Prokić, Marko, Zaletel, Ivan, Todorović, Zoran, "The effect of long-term high-dose coconut oil supplementation on rat sliver and serum lipids" in BIT´s 6th Annual World Congress of Food and Nutrition: Abstract Book. Shenyang, China; September 15-17, 2017 (2017):168,
https://hdl.handle.net/21.15107/rcub_ibiss_3423 .

TY  - CONF
AU  - Đurašević, Siniša
AU  - Jasnić, Nebojša
AU  - Dakić, Tamara
AU  - Jevđović, Tanja
AU  - Lakić, Iva
AU  - Vujović, Predrag
AU  - Đorđević, Jelena
AU  - Mitić-Ćulafić, Dragana
AU  - Nikolić, Biljana
AU  - Grigorov, Ilijana
AU  - Bogojević, Desanka
AU  - Pavlović, Slađan
AU  - Prokić, Marko
AU  - Zaletel, Ivan
AU  - Todorović, Zoran
PY  - 2017
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3422
AB  - We investigated the effect of long-term high-dose virgin coconut oil (VCO) supplementation on rat glucose homeostasis. Animals were divided into two groups with 6 of them in each: normally fed (Control group) and the group fed with coconut oil at a concentration of 20% in food (VCO group). The experiment lasted for four months. We measured fasting glycemia once a week during the entire experiment. In the last week of the experiment, we performed an oral glucose tolerance test (OGTT) and an intraperitoneal insulin tolerance test (ITT). On the last day of the experiment the fasting insulin and glyc8mia were measured in the blood of animals. The results show that coconut oil reduces weekly glycemia in VCO animals compared with controls. This effect reaches its maximum after the first two weeks of the experiment, and then slowly decreases and disappears over time of next eight weeks. As a result, the glycemia of control and VCO animals do not differ in last six weeks of the experiment. The area under the curve (AUC) presenting glycemia during whole the experiment is significantly lower in VCO animals than in the controls. The hypoglycemic effect of coconut oil is obviously dose-dependent since the amount of food (and therefore the coconut oil) that the animals eat decreases over the time. The results of the oral glucose tolerance test show that the OGTT AUC of VCO animals is significantly lower than the controls, and same is true for the insulin tolerance test. Finally, glycemia and insulin concentration in serums sampled on the last day of the experiment do not differ between VCO and Control groups, so accordingly neither HOMA-IR I and 2 (Homeostatic model assessment of insulin resistance) nor QUIC.Kl ( Quantitative Insulin Sensitivity Check Index). In conclusion, our results show beneficial effects of long-term high-dose coconut oil supplementation on rat glucose homeostasis.
PB  - BIT Congress Inc. (BIT Group Global Ltd.)
C3  - BIT´s 6th Annual World Congress of Food and Nutrition: Abstract Book. Shenyang, China; September 15-17, 2017
T1  - The effect of long-term high-dose coconut oil supplementation on rat glucose homeostasis
SP  - 167
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_3422
ER  - 

@conference{
author = "Đurašević, Siniša and Jasnić, Nebojša and Dakić, Tamara and Jevđović, Tanja and Lakić, Iva and Vujović, Predrag and Đorđević, Jelena and Mitić-Ćulafić, Dragana and Nikolić, Biljana and Grigorov, Ilijana and Bogojević, Desanka and Pavlović, Slađan and Prokić, Marko and Zaletel, Ivan and Todorović, Zoran",
year = "2017",
abstract = "We investigated the effect of long-term high-dose virgin coconut oil (VCO) supplementation on rat glucose homeostasis. Animals were divided into two groups with 6 of them in each: normally fed (Control group) and the group fed with coconut oil at a concentration of 20% in food (VCO group). The experiment lasted for four months. We measured fasting glycemia once a week during the entire experiment. In the last week of the experiment, we performed an oral glucose tolerance test (OGTT) and an intraperitoneal insulin tolerance test (ITT). On the last day of the experiment the fasting insulin and glyc8mia were measured in the blood of animals. The results show that coconut oil reduces weekly glycemia in VCO animals compared with controls. This effect reaches its maximum after the first two weeks of the experiment, and then slowly decreases and disappears over time of next eight weeks. As a result, the glycemia of control and VCO animals do not differ in last six weeks of the experiment. The area under the curve (AUC) presenting glycemia during whole the experiment is significantly lower in VCO animals than in the controls. The hypoglycemic effect of coconut oil is obviously dose-dependent since the amount of food (and therefore the coconut oil) that the animals eat decreases over the time. The results of the oral glucose tolerance test show that the OGTT AUC of VCO animals is significantly lower than the controls, and same is true for the insulin tolerance test. Finally, glycemia and insulin concentration in serums sampled on the last day of the experiment do not differ between VCO and Control groups, so accordingly neither HOMA-IR I and 2 (Homeostatic model assessment of insulin resistance) nor QUIC.Kl ( Quantitative Insulin Sensitivity Check Index). In conclusion, our results show beneficial effects of long-term high-dose coconut oil supplementation on rat glucose homeostasis.",
publisher = "BIT Congress Inc. (BIT Group Global Ltd.)",
journal = "BIT´s 6th Annual World Congress of Food and Nutrition: Abstract Book. Shenyang, China; September 15-17, 2017",
title = "The effect of long-term high-dose coconut oil supplementation on rat glucose homeostasis",
pages = "167",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_3422"
}

Đurašević, S., Jasnić, N., Dakić, T., Jevđović, T., Lakić, I., Vujović, P., Đorđević, J., Mitić-Ćulafić, D., Nikolić, B., Grigorov, I., Bogojević, D., Pavlović, S., Prokić, M., Zaletel, I.,& Todorović, Z.. (2017). The effect of long-term high-dose coconut oil supplementation on rat glucose homeostasis. in BIT´s 6th Annual World Congress of Food and Nutrition: Abstract Book. Shenyang, China; September 15-17, 2017
BIT Congress Inc. (BIT Group Global Ltd.)., 167.
https://hdl.handle.net/21.15107/rcub_ibiss_3422

Đurašević S, Jasnić N, Dakić T, Jevđović T, Lakić I, Vujović P, Đorđević J, Mitić-Ćulafić D, Nikolić B, Grigorov I, Bogojević D, Pavlović S, Prokić M, Zaletel I, Todorović Z. The effect of long-term high-dose coconut oil supplementation on rat glucose homeostasis. in BIT´s 6th Annual World Congress of Food and Nutrition: Abstract Book. Shenyang, China; September 15-17, 2017. 2017;:167.
https://hdl.handle.net/21.15107/rcub_ibiss_3422 .

Đurašević, Siniša, Jasnić, Nebojša, Dakić, Tamara, Jevđović, Tanja, Lakić, Iva, Vujović, Predrag, Đorđević, Jelena, Mitić-Ćulafić, Dragana, Nikolić, Biljana, Grigorov, Ilijana, Bogojević, Desanka, Pavlović, Slađan, Prokić, Marko, Zaletel, Ivan, Todorović, Zoran, "The effect of long-term high-dose coconut oil supplementation on rat glucose homeostasis" in BIT´s 6th Annual World Congress of Food and Nutrition: Abstract Book. Shenyang, China; September 15-17, 2017 (2017):167,
https://hdl.handle.net/21.15107/rcub_ibiss_3422 .

TY  - JOUR
AU  - Matić, Sanja
AU  - Stanić, Snežana
AU  - Mihailović, Mirjana
AU  - Bogojević, Desanka
PY  - 2016
UR  - http://www.sciencedirect.com/science/article/pii/S1319562X15001138
UR  - http://linkinghub.elsevier.com/retrieve/pii/S1319562X15001138
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3177
AB  - The Anacardiaceae Lindl. family comprises of many species which are used in nutrition and in traditional folk medicine for the treatment of several human diseases. Cotinus coggygria Scop. commonly known as “smoke tree”, is an commercial ornamental plant with high medicinal usages, belongs to the family Anacardiaceae. The present review provides a comprehensive report of empirical investigations on important pharmacological activities and phytochemical screening of essential oils and extracts. Relevant information was collected from scientific journals, books, and reports via library and electronic search using Medline, Pubmed, Google Scholar, ScienceDirect, Web of Science, and Scopus. The plant has been extensively investigated in a broad range of studies to provide scientific evidence for folklore claims or to find new therapeutic uses. Numerous activities namely antioxidative, antibacterial, antifungal, antiviral, anticancer, antigenotoxic, hepatoprotective and anti-inflammatory have been demonstrated for all parts of these plants by in vivo and in vitro studies. Essential oils and extracts showed various pharmacological and biological properties which make them an effective remedy for various kinds of illnesses. Considering data from the literature, it could be demonstrated that C. coggygria possesses diverse bioactive properties and immense utilization in medicine, health care, cosmetics and as health supplements.
T2  - Saudi Journal of Biological Sciences
T1  - Cotinus coggygria Scop.: An overview of its chemical constituents, pharmacological and toxicological potential
IS  - 4
VL  - 23
DO  - 10.1016/j.sjbs.2015.05.012
SP  - 452
EP  - 461
ER  - 

@article{
author = "Matić, Sanja and Stanić, Snežana and Mihailović, Mirjana and Bogojević, Desanka",
year = "2016",
abstract = "The Anacardiaceae Lindl. family comprises of many species which are used in nutrition and in traditional folk medicine for the treatment of several human diseases. Cotinus coggygria Scop. commonly known as “smoke tree”, is an commercial ornamental plant with high medicinal usages, belongs to the family Anacardiaceae. The present review provides a comprehensive report of empirical investigations on important pharmacological activities and phytochemical screening of essential oils and extracts. Relevant information was collected from scientific journals, books, and reports via library and electronic search using Medline, Pubmed, Google Scholar, ScienceDirect, Web of Science, and Scopus. The plant has been extensively investigated in a broad range of studies to provide scientific evidence for folklore claims or to find new therapeutic uses. Numerous activities namely antioxidative, antibacterial, antifungal, antiviral, anticancer, antigenotoxic, hepatoprotective and anti-inflammatory have been demonstrated for all parts of these plants by in vivo and in vitro studies. Essential oils and extracts showed various pharmacological and biological properties which make them an effective remedy for various kinds of illnesses. Considering data from the literature, it could be demonstrated that C. coggygria possesses diverse bioactive properties and immense utilization in medicine, health care, cosmetics and as health supplements.",
journal = "Saudi Journal of Biological Sciences",
title = "Cotinus coggygria Scop.: An overview of its chemical constituents, pharmacological and toxicological potential",
number = "4",
volume = "23",
doi = "10.1016/j.sjbs.2015.05.012",
pages = "452-461"
}

Matić, S., Stanić, S., Mihailović, M.,& Bogojević, D.. (2016). Cotinus coggygria Scop.: An overview of its chemical constituents, pharmacological and toxicological potential. in Saudi Journal of Biological Sciences, 23(4), 452-461.
https://doi.org/10.1016/j.sjbs.2015.05.012

Matić S, Stanić S, Mihailović M, Bogojević D. Cotinus coggygria Scop.: An overview of its chemical constituents, pharmacological and toxicological potential. in Saudi Journal of Biological Sciences. 2016;23(4):452-461.
doi:10.1016/j.sjbs.2015.05.012 .

Matić, Sanja, Stanić, Snežana, Mihailović, Mirjana, Bogojević, Desanka, "Cotinus coggygria Scop.: An overview of its chemical constituents, pharmacological and toxicological potential" in Saudi Journal of Biological Sciences, 23, no. 4 (2016):452-461,
https://doi.org/10.1016/j.sjbs.2015.05.012 . .

TY  - CONF
AU  - Petrović, Anja
AU  - Bogojević, Desanka
AU  - Ivanović Matić, Svetlana
AU  - Martinović, Vesna
AU  - Jovanović Stojanov, Sofija
AU  - Stevanović, Jelena
AU  - Blagojević, Duško
AU  - Grigorov, Ilijana
PY  - 2016
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4280
AB  - Melatonin, a hormone secreted primarly by pineal gland,exhibitsantioxidative and anti-inflammatory properties. We have previously reported antinecrotic effect of melatonin in the liver of streptozotocin (STZ) treated rats. However, molecular mechanisms underlyingmelatonin hepatoprotective rolein oxidative enviroment are still partially known. In this study we investigated effects of melatonin on the role of nuclear factor-kappa B (NF-κB) p65 and nuclear erythroid 2-related factor 2 (Nrf2) in the liver of STZ treated rats.Melatonin at doses of 2 mg/kg/i.p was administrated daily, 3 days before STZ treatment (65mg/kg, i.p), and continued until the end of study at 4 weeks after STZ injection. STZ treatment causeshypoinsulinemia followed by hyperglycemia which increases the production of reactive oxidative species (ROS) leading tooxidative stress. ROS activatedNF-κB p65 in hepatocytes and increased its nuclear expresssion where it enhances expression of genes of proinflammatory cytokines leading to elevated presence of TNFα and IL-6. High TNFα has a cytotoxic activity and may potentiate liver damage.Melatonin reduced the elevated expression of NF-κB p65, TNFα and IL-6.STZ treatmentincreased expression of Nrf2 but reduced its activation which is followed by decrease in superoxide dismutase (SOD), glutathione-S-transferase (GST) and catalase (CAT) expression and activity. Melatonin significantly increases nuclear expression of Nrf2 which enhances the up-regulation of SOD, GST and CAT expression and activity.The results of this study suggest that melatonin improves oxidative–induced liver damage by attenuation of proinflammatory stimuli through decreasing of NF-κB activation cascade and strengthens antioxidative defence through activation of Nrf2 cascade.
PB  - Bratislava: Institute of Normal and Pathological Physiology, Slovak Academy of Sciences
C3  - 2nd Joint Meeting of Slovak and Serbian Physiological Societies “Physiology Without Frontiers“, Book of Abstracts
T1  - Melatonin attenuates streptozotocin induced inflammation and oxidative stress in the rat liver by modulation of NF-kB and Nrf2 signaling
SP  - 39
EP  - 39
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_4280
ER  - 

@conference{
author = "Petrović, Anja and Bogojević, Desanka and Ivanović Matić, Svetlana and Martinović, Vesna and Jovanović Stojanov, Sofija and Stevanović, Jelena and Blagojević, Duško and Grigorov, Ilijana",
year = "2016",
abstract = "Melatonin, a hormone secreted primarly by pineal gland,exhibitsantioxidative and anti-inflammatory properties. We have previously reported antinecrotic effect of melatonin in the liver of streptozotocin (STZ) treated rats. However, molecular mechanisms underlyingmelatonin hepatoprotective rolein oxidative enviroment are still partially known. In this study we investigated effects of melatonin on the role of nuclear factor-kappa B (NF-κB) p65 and nuclear erythroid 2-related factor 2 (Nrf2) in the liver of STZ treated rats.Melatonin at doses of 2 mg/kg/i.p was administrated daily, 3 days before STZ treatment (65mg/kg, i.p), and continued until the end of study at 4 weeks after STZ injection. STZ treatment causeshypoinsulinemia followed by hyperglycemia which increases the production of reactive oxidative species (ROS) leading tooxidative stress. ROS activatedNF-κB p65 in hepatocytes and increased its nuclear expresssion where it enhances expression of genes of proinflammatory cytokines leading to elevated presence of TNFα and IL-6. High TNFα has a cytotoxic activity and may potentiate liver damage.Melatonin reduced the elevated expression of NF-κB p65, TNFα and IL-6.STZ treatmentincreased expression of Nrf2 but reduced its activation which is followed by decrease in superoxide dismutase (SOD), glutathione-S-transferase (GST) and catalase (CAT) expression and activity. Melatonin significantly increases nuclear expression of Nrf2 which enhances the up-regulation of SOD, GST and CAT expression and activity.The results of this study suggest that melatonin improves oxidative–induced liver damage by attenuation of proinflammatory stimuli through decreasing of NF-κB activation cascade and strengthens antioxidative defence through activation of Nrf2 cascade.",
publisher = "Bratislava: Institute of Normal and Pathological Physiology, Slovak Academy of Sciences",
journal = "2nd Joint Meeting of Slovak and Serbian Physiological Societies “Physiology Without Frontiers“, Book of Abstracts",
title = "Melatonin attenuates streptozotocin induced inflammation and oxidative stress in the rat liver by modulation of NF-kB and Nrf2 signaling",
pages = "39-39",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_4280"
}

Petrović, A., Bogojević, D., Ivanović Matić, S., Martinović, V., Jovanović Stojanov, S., Stevanović, J., Blagojević, D.,& Grigorov, I.. (2016). Melatonin attenuates streptozotocin induced inflammation and oxidative stress in the rat liver by modulation of NF-kB and Nrf2 signaling. in 2nd Joint Meeting of Slovak and Serbian Physiological Societies “Physiology Without Frontiers“, Book of Abstracts
Bratislava: Institute of Normal and Pathological Physiology, Slovak Academy of Sciences., 39-39.
https://hdl.handle.net/21.15107/rcub_ibiss_4280

Petrović A, Bogojević D, Ivanović Matić S, Martinović V, Jovanović Stojanov S, Stevanović J, Blagojević D, Grigorov I. Melatonin attenuates streptozotocin induced inflammation and oxidative stress in the rat liver by modulation of NF-kB and Nrf2 signaling. in 2nd Joint Meeting of Slovak and Serbian Physiological Societies “Physiology Without Frontiers“, Book of Abstracts. 2016;:39-39.
https://hdl.handle.net/21.15107/rcub_ibiss_4280 .

Petrović, Anja, Bogojević, Desanka, Ivanović Matić, Svetlana, Martinović, Vesna, Jovanović Stojanov, Sofija, Stevanović, Jelena, Blagojević, Duško, Grigorov, Ilijana, "Melatonin attenuates streptozotocin induced inflammation and oxidative stress in the rat liver by modulation of NF-kB and Nrf2 signaling" in 2nd Joint Meeting of Slovak and Serbian Physiological Societies “Physiology Without Frontiers“, Book of Abstracts (2016):39-39,
https://hdl.handle.net/21.15107/rcub_ibiss_4280 .

TY  - CONF
AU  - Petrović, Anja
AU  - Bogojević, Desanka
AU  - Ivanović-Matić, Svetlana
AU  - Martinović, Vesna
AU  - Korać, Aleksandra
AU  - Jovanović-Stojanov, Sofija
AU  - Stevanović, Jelena
AU  - Poznanović, Goran
AU  - Grigorov, Ilijana
PY  - 2015
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5654
AB  - Autophagy is a cellular process that involves lysosomal degradation and recycling of intracellular
organelles and proteins. By removing damaged and dysfunctional cellular components in order to
maintain energy homeostasis during cellular stress, autophagy can serve as a cytoprotective
mechanism. Also, it could lead to cell death if it‟s overactive or defective. Molecular mechanisms
responsible for the two faces of autophagy are still partially known. Therefore, for the development of
therapy based on autophagy modulation, it‟s necessary to fully define these processes. This study
investigated the role of oxidative stress on autophagic processes in the liver of diabetic rats and effects
of melatonin, as an antioxidant, on autophagy initiation/modulation. The liver, as one of the main
target organs of insulin, takes an important role in regulation of glucose homeostasis. In diabetes,
hypoinsulinemia followed by hyperglycemia increases mitochondrial proton gradient within the cells.
In this state organelles become the source of reactive oxidative species leading to macromolecule
damage which may cause necrotic, apoptotic or autophagic cell death. In the liver of diabetic rats
obtained four weeks after diabetes induction with streptozotocin (65 mg/kg, i.p.), light and electron
transmission microscopy showed significant changes in the structure of the cells and a large number of
necrotic cells. By using Western blot, immunoprecipitation and confocal microscopy analyses,
autophagy in diabetic liver was confirmed by increased expression of proteins required for
autophagosome formation, LC3B and Beclin1, and by the presence of Beclin1 interactions with its
activator HMGB1. In the state of oxidative stress HMGB1 is relocated from the nucleus to the
cytoplasm. Continuous melatonin treatment of diabetic rats (2mg/kg/daily, i.p.) leads to significant
reduction of liver damage, presumably through elevated mitochondrial autophagy. Melatonin
additionally contributes to elevated expression of LC3B and Beclin1, HMGB1-Beclin1 interactions
and autophagosome formation. Thus, it seems that melatonin protects the liver from diabetes induced
damage by favoring autophagy as a protective mechanism.
PB  - Belgrade : Serbian Society for Mitochondrial and Free-Radical Physiology
C3  - Book of Abstracts: Third Congress Redox Medicine: Reactive Species Signaling, Analytical Methods, Phytopharmacy, Molecular Mechanisms of Disease - SSMFRP-2015; 2015 Sep 25-26; Belgrade, Serbia
T1  - Effects of melatonin on autophagic processes in the liver of diabetic rats
SP  - 33
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5654
ER  - 

@conference{
author = "Petrović, Anja and Bogojević, Desanka and Ivanović-Matić, Svetlana and Martinović, Vesna and Korać, Aleksandra and Jovanović-Stojanov, Sofija and Stevanović, Jelena and Poznanović, Goran and Grigorov, Ilijana",
year = "2015",
abstract = "Autophagy is a cellular process that involves lysosomal degradation and recycling of intracellular
organelles and proteins. By removing damaged and dysfunctional cellular components in order to
maintain energy homeostasis during cellular stress, autophagy can serve as a cytoprotective
mechanism. Also, it could lead to cell death if it‟s overactive or defective. Molecular mechanisms
responsible for the two faces of autophagy are still partially known. Therefore, for the development of
therapy based on autophagy modulation, it‟s necessary to fully define these processes. This study
investigated the role of oxidative stress on autophagic processes in the liver of diabetic rats and effects
of melatonin, as an antioxidant, on autophagy initiation/modulation. The liver, as one of the main
target organs of insulin, takes an important role in regulation of glucose homeostasis. In diabetes,
hypoinsulinemia followed by hyperglycemia increases mitochondrial proton gradient within the cells.
In this state organelles become the source of reactive oxidative species leading to macromolecule
damage which may cause necrotic, apoptotic or autophagic cell death. In the liver of diabetic rats
obtained four weeks after diabetes induction with streptozotocin (65 mg/kg, i.p.), light and electron
transmission microscopy showed significant changes in the structure of the cells and a large number of
necrotic cells. By using Western blot, immunoprecipitation and confocal microscopy analyses,
autophagy in diabetic liver was confirmed by increased expression of proteins required for
autophagosome formation, LC3B and Beclin1, and by the presence of Beclin1 interactions with its
activator HMGB1. In the state of oxidative stress HMGB1 is relocated from the nucleus to the
cytoplasm. Continuous melatonin treatment of diabetic rats (2mg/kg/daily, i.p.) leads to significant
reduction of liver damage, presumably through elevated mitochondrial autophagy. Melatonin
additionally contributes to elevated expression of LC3B and Beclin1, HMGB1-Beclin1 interactions
and autophagosome formation. Thus, it seems that melatonin protects the liver from diabetes induced
damage by favoring autophagy as a protective mechanism.",
publisher = "Belgrade : Serbian Society for Mitochondrial and Free-Radical Physiology",
journal = "Book of Abstracts: Third Congress Redox Medicine: Reactive Species Signaling, Analytical Methods, Phytopharmacy, Molecular Mechanisms of Disease - SSMFRP-2015; 2015 Sep 25-26; Belgrade, Serbia",
title = "Effects of melatonin on autophagic processes in the liver of diabetic rats",
pages = "33",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5654"
}

Petrović, A., Bogojević, D., Ivanović-Matić, S., Martinović, V., Korać, A., Jovanović-Stojanov, S., Stevanović, J., Poznanović, G.,& Grigorov, I.. (2015). Effects of melatonin on autophagic processes in the liver of diabetic rats. in Book of Abstracts: Third Congress Redox Medicine: Reactive Species Signaling, Analytical Methods, Phytopharmacy, Molecular Mechanisms of Disease - SSMFRP-2015; 2015 Sep 25-26; Belgrade, Serbia
Belgrade : Serbian Society for Mitochondrial and Free-Radical Physiology., 33.
https://hdl.handle.net/21.15107/rcub_ibiss_5654

Petrović A, Bogojević D, Ivanović-Matić S, Martinović V, Korać A, Jovanović-Stojanov S, Stevanović J, Poznanović G, Grigorov I. Effects of melatonin on autophagic processes in the liver of diabetic rats. in Book of Abstracts: Third Congress Redox Medicine: Reactive Species Signaling, Analytical Methods, Phytopharmacy, Molecular Mechanisms of Disease - SSMFRP-2015; 2015 Sep 25-26; Belgrade, Serbia. 2015;:33.
https://hdl.handle.net/21.15107/rcub_ibiss_5654 .

Petrović, Anja, Bogojević, Desanka, Ivanović-Matić, Svetlana, Martinović, Vesna, Korać, Aleksandra, Jovanović-Stojanov, Sofija, Stevanović, Jelena, Poznanović, Goran, Grigorov, Ilijana, "Effects of melatonin on autophagic processes in the liver of diabetic rats" in Book of Abstracts: Third Congress Redox Medicine: Reactive Species Signaling, Analytical Methods, Phytopharmacy, Molecular Mechanisms of Disease - SSMFRP-2015; 2015 Sep 25-26; Belgrade, Serbia (2015):33,
https://hdl.handle.net/21.15107/rcub_ibiss_5654 .

TY  - CONF
AU  - Mihailović, Mirjana
AU  - Petrović, Miodrag
AU  - Grdović, Nevena
AU  - Dinić, Svetlana
AU  - Uskoković, Aleksandra
AU  - Vidaković, Melita
AU  - Grigorov, Ilijana
AU  - Bogojević, Desanka
AU  - Ivanović-Matić, Svetlana
AU  - Martinović, Vesna
AU  - Arambašić Jovanović, Jelena
AU  - Poznanović, Goran
PY  - 2014
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5653
AB  - Metallothioneins (MTs) constitute a family of low-molecular  weight, cysteine­ rich and heat stable 
proteins involved in the binding and regulation of essential metals, such as copper and zinc, and 
in the detoxification of these and other non-essential metals, such as cadmium and mercury. 
Previously we showed that the induction of MTs in Merluccius merluccius and Mui/us barbatus 
correlated with elevated concentrations of Cu and Pb, determined by chemical analysis of the 
seawater from Bar and Valdanos. In the present study we studied protein expression of MTs in the 
hepatopancreas of several seawater fish species: Red mullet (Mui/us barbatus), European hake 
(Merluccius merluccius), Tub gurnard (Trig/a lucerna) and Thinlip mullet  (Liza ramada), from the 
Monetengrin Adriatic coastline. Western blot analysis revealed the highest induction of MTs in the 
hepatopancreas in the following order: Merluccius merluccius, Trig/a lucerna, Mui/us barbatus and 
Liza ramada. Considering that MTs play a role in the metabolism of essential metals, they  are 
constitutively expressed. The presence of elevated concentrations of both essential and toxic 
metals provokes the induction of MTs. These results are in correlation with literature data showing 
that fish species differ in their detoxification capacities and amounts of accumulated  metals.  We 
 conclude that the level of induction of MTs in the hepatopancreas of the examined fish species 
correlates with the level of their reliability as bioindicator species in heavy metal 
biomonitoring.
PB  - Kotor, Montenegro : University of Montenegro, Institute of Marine Biology
C3  - Book of Abstracts: 1st International scientific conference integrated coastal zone management in the Adriatic sea; 2014 Sep 29 - Oct 1; Kotor, Montenegro
T1  - Species-specific expression of metallothionein in the hepatopancreas of seawater fish from the Montenegrin Adriatic coastline
SP  - 28
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5653
ER  - 

@conference{
author = "Mihailović, Mirjana and Petrović, Miodrag and Grdović, Nevena and Dinić, Svetlana and Uskoković, Aleksandra and Vidaković, Melita and Grigorov, Ilijana and Bogojević, Desanka and Ivanović-Matić, Svetlana and Martinović, Vesna and Arambašić Jovanović, Jelena and Poznanović, Goran",
year = "2014",
abstract = "Metallothioneins (MTs) constitute a family of low-molecular  weight, cysteine­ rich and heat stable 
proteins involved in the binding and regulation of essential metals, such as copper and zinc, and 
in the detoxification of these and other non-essential metals, such as cadmium and mercury. 
Previously we showed that the induction of MTs in Merluccius merluccius and Mui/us barbatus 
correlated with elevated concentrations of Cu and Pb, determined by chemical analysis of the 
seawater from Bar and Valdanos. In the present study we studied protein expression of MTs in the 
hepatopancreas of several seawater fish species: Red mullet (Mui/us barbatus), European hake 
(Merluccius merluccius), Tub gurnard (Trig/a lucerna) and Thinlip mullet  (Liza ramada), from the 
Monetengrin Adriatic coastline. Western blot analysis revealed the highest induction of MTs in the 
hepatopancreas in the following order: Merluccius merluccius, Trig/a lucerna, Mui/us barbatus and 
Liza ramada. Considering that MTs play a role in the metabolism of essential metals, they  are 
constitutively expressed. The presence of elevated concentrations of both essential and toxic 
metals provokes the induction of MTs. These results are in correlation with literature data showing 
that fish species differ in their detoxification capacities and amounts of accumulated  metals.  We 
 conclude that the level of induction of MTs in the hepatopancreas of the examined fish species 
correlates with the level of their reliability as bioindicator species in heavy metal 
biomonitoring.",
publisher = "Kotor, Montenegro : University of Montenegro, Institute of Marine Biology",
journal = "Book of Abstracts: 1st International scientific conference integrated coastal zone management in the Adriatic sea; 2014 Sep 29 - Oct 1; Kotor, Montenegro",
title = "Species-specific expression of metallothionein in the hepatopancreas of seawater fish from the Montenegrin Adriatic coastline",
pages = "28",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5653"
}

Mihailović, M., Petrović, M., Grdović, N., Dinić, S., Uskoković, A., Vidaković, M., Grigorov, I., Bogojević, D., Ivanović-Matić, S., Martinović, V., Arambašić Jovanović, J.,& Poznanović, G.. (2014). Species-specific expression of metallothionein in the hepatopancreas of seawater fish from the Montenegrin Adriatic coastline. in Book of Abstracts: 1st International scientific conference integrated coastal zone management in the Adriatic sea; 2014 Sep 29 - Oct 1; Kotor, Montenegro
Kotor, Montenegro : University of Montenegro, Institute of Marine Biology., 28.
https://hdl.handle.net/21.15107/rcub_ibiss_5653

Mihailović M, Petrović M, Grdović N, Dinić S, Uskoković A, Vidaković M, Grigorov I, Bogojević D, Ivanović-Matić S, Martinović V, Arambašić Jovanović J, Poznanović G. Species-specific expression of metallothionein in the hepatopancreas of seawater fish from the Montenegrin Adriatic coastline. in Book of Abstracts: 1st International scientific conference integrated coastal zone management in the Adriatic sea; 2014 Sep 29 - Oct 1; Kotor, Montenegro. 2014;:28.
https://hdl.handle.net/21.15107/rcub_ibiss_5653 .

Mihailović, Mirjana, Petrović, Miodrag, Grdović, Nevena, Dinić, Svetlana, Uskoković, Aleksandra, Vidaković, Melita, Grigorov, Ilijana, Bogojević, Desanka, Ivanović-Matić, Svetlana, Martinović, Vesna, Arambašić Jovanović, Jelena, Poznanović, Goran, "Species-specific expression of metallothionein in the hepatopancreas of seawater fish from the Montenegrin Adriatic coastline" in Book of Abstracts: 1st International scientific conference integrated coastal zone management in the Adriatic sea; 2014 Sep 29 - Oct 1; Kotor, Montenegro (2014):28,
https://hdl.handle.net/21.15107/rcub_ibiss_5653 .

TY  - JOUR
AU  - Grigorov, Ilijana
AU  - Bogojević, Desanka
AU  - Jovanović Stojanov, Sofija
AU  - Petrović, Anja
AU  - Ivanović Matić, Svetlana
AU  - Zolotarevski, Lidija
AU  - Poznanović, Goran
AU  - Martinović, Vesna
PY  - 2014
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2210
AB  - Oxidative stress-mediated damage to liver tissue underlies the
   pathological alterations in liver morphology and function that are
   observed in diabetes. We examined the effects of the antioxidant action
   of melatonin against necrosis-inducing DNA damage in hepatocytes of
   streptozotocin (STZ)-induced diabetic rats. Daily administration of
   melatonin (0.2 mg/kg) was initiated 3 days before diabetes induction and
   maintained for 4 weeks. Melatonin-treated diabetic rats exhibited
   improved markers of liver injury (P<0.05), alkaline phosphatase, and
   alanine and aspartate aminotransferases. Melatonin prevented the
   diabetes-related morphological deterioration of hepatocytes, DNA damage
   (P<0.05), and hepatocellular necrosis. The improvement was due to
   containment of the pronecrotic oxygen radical load, observed as
   inhibition (P<0.05) of the diabetes-induced rise in lipid peroxidation
   and hydrogen peroxide increase in the liver. This was accompanied by
   improved necrotic markers of cellular damage: a significant reduction in
   cleavage of the DNA repair enzyme poly(ADP-ribose) polymerase 1 (PARP-1)
   into necrotic 55- and 62-kDa fragments, and inhibition of
   nucleus-to-cytoplasm translocation and accumulation in the serum of the
   high-mobility group box 1 (HMGB1) protein. We conclude that melatonin is
   hepatoprotective in diabetes. It reduces extensive DNA damage and
   resulting necrotic processes. Melatonin application could thus present a
   viable therapeutic option in the management of diabetes-induced liver
   injury.
T2  - Journal of Physiology and Biochemistry
T1  - Hepatoprotective effects of melatonin against pronecrotic cellular
 events in streptozotocin-induced diabetic rats
IS  - 2
VL  - 70
DO  - 10.1007/s13105-014-0322-7
SP  - 441
EP  - 450
ER  - 

@article{
author = "Grigorov, Ilijana and Bogojević, Desanka and Jovanović Stojanov, Sofija and Petrović, Anja and Ivanović Matić, Svetlana and Zolotarevski, Lidija and Poznanović, Goran and Martinović, Vesna",
year = "2014",
abstract = "Oxidative stress-mediated damage to liver tissue underlies the
   pathological alterations in liver morphology and function that are
   observed in diabetes. We examined the effects of the antioxidant action
   of melatonin against necrosis-inducing DNA damage in hepatocytes of
   streptozotocin (STZ)-induced diabetic rats. Daily administration of
   melatonin (0.2 mg/kg) was initiated 3 days before diabetes induction and
   maintained for 4 weeks. Melatonin-treated diabetic rats exhibited
   improved markers of liver injury (P<0.05), alkaline phosphatase, and
   alanine and aspartate aminotransferases. Melatonin prevented the
   diabetes-related morphological deterioration of hepatocytes, DNA damage
   (P<0.05), and hepatocellular necrosis. The improvement was due to
   containment of the pronecrotic oxygen radical load, observed as
   inhibition (P<0.05) of the diabetes-induced rise in lipid peroxidation
   and hydrogen peroxide increase in the liver. This was accompanied by
   improved necrotic markers of cellular damage: a significant reduction in
   cleavage of the DNA repair enzyme poly(ADP-ribose) polymerase 1 (PARP-1)
   into necrotic 55- and 62-kDa fragments, and inhibition of
   nucleus-to-cytoplasm translocation and accumulation in the serum of the
   high-mobility group box 1 (HMGB1) protein. We conclude that melatonin is
   hepatoprotective in diabetes. It reduces extensive DNA damage and
   resulting necrotic processes. Melatonin application could thus present a
   viable therapeutic option in the management of diabetes-induced liver
   injury.",
journal = "Journal of Physiology and Biochemistry",
title = "Hepatoprotective effects of melatonin against pronecrotic cellular
 events in streptozotocin-induced diabetic rats",
number = "2",
volume = "70",
doi = "10.1007/s13105-014-0322-7",
pages = "441-450"
}

Grigorov, I., Bogojević, D., Jovanović Stojanov, S., Petrović, A., Ivanović Matić, S., Zolotarevski, L., Poznanović, G.,& Martinović, V.. (2014). Hepatoprotective effects of melatonin against pronecrotic cellular
 events in streptozotocin-induced diabetic rats. in Journal of Physiology and Biochemistry, 70(2), 441-450.
https://doi.org/10.1007/s13105-014-0322-7

Grigorov I, Bogojević D, Jovanović Stojanov S, Petrović A, Ivanović Matić S, Zolotarevski L, Poznanović G, Martinović V. Hepatoprotective effects of melatonin against pronecrotic cellular
 events in streptozotocin-induced diabetic rats. in Journal of Physiology and Biochemistry. 2014;70(2):441-450.
doi:10.1007/s13105-014-0322-7 .

Grigorov, Ilijana, Bogojević, Desanka, Jovanović Stojanov, Sofija, Petrović, Anja, Ivanović Matić, Svetlana, Zolotarevski, Lidija, Poznanović, Goran, Martinović, Vesna, "Hepatoprotective effects of melatonin against pronecrotic cellular
 events in streptozotocin-induced diabetic rats" in Journal of Physiology and Biochemistry, 70, no. 2 (2014):441-450,
https://doi.org/10.1007/s13105-014-0322-7 . .

TY  - JOUR
AU  - Ivanović Matić, Svetlana
AU  - Bogojević, Desanka
AU  - Martinović, Vesna
AU  - Petrovic, Anja
AU  - Jovanovic-Stojanov, Sofija
AU  - Poznanović, Goran
AU  - Grigorov, Ilijana
PY  - 2014
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2117
AB  - Diabetes is a risk factor for cardiovascular disease that has a
   multifactorial etiology, with oxidative stress as an important
   component. Our previous observation of a significant diabetes-related
   increase in rat cardiac catalase (CAT) activity suggested that CAT could
   play a major role in delaying the development of diabetic
   cardiomyopathy. Thus, in the present work, we examined the effects of
   the daily administration of the CAT inhibitor, 3-amino-1,2,4-triazole (1
   mg/g), on the hearts of streptozotocin (STZ)-induced diabetic rats.
   Administration of CAT inhibitor was started from the 15th day after the
   last STZ treatment (40 mg/kg/5 days), and maintained until the end of
   the 4th or 6th weeks of diabetes. Compared to untreated diabetic rats,
   at the end of the observation period, CAT inhibition lowered the induced
   level of cardiac CAT activity to the basal level and decreased CAT
   protein expression, mediated through a decline in the nuclear factor
   erythroid-derived 2-like 2 /nuclear factor-kappa B p65 (Nrf2/NF-kappa B
   p65) subunit ratio. The perturbed antioxidant defenses resulting from
   CAT inhibition promoted increased H2O2 production (P < 0.05) and lipid
   peroxidation (P < 0.05). Generated cytotoxic stimuli increased DNA
   damage (P < 0.05) and activated pro-apoptotic events, observed as a
   decrease (P < 0.05) in the ratio of the apoptosis regulator proteins
   Bcl-2/Bax, increased (P < 0.05) presence of the poly(ADP-ribose)
   polymerase-1 (PARP-1) 85 kDa apoptotic fragment and cytoplasmic levels
   of cytochrome C. These findings confirm an important function of CAT in
   the suppression of events leading to diabetes-promoted cardiac
   dysfunction and cardiomyopathy.
T2  - Journal of Physiology and Biochemistry
T1  - Catalase inhibition in diabetic rats potentiates DNA damage and
 apoptotic cell death setting the stage for cardiomyopathy
IS  - 4
VL  - 70
DO  - 10.1007/s13105-014-0363-y
SP  - 947
EP  - 959
ER  - 

@article{
author = "Ivanović Matić, Svetlana and Bogojević, Desanka and Martinović, Vesna and Petrovic, Anja and Jovanovic-Stojanov, Sofija and Poznanović, Goran and Grigorov, Ilijana",
year = "2014",
abstract = "Diabetes is a risk factor for cardiovascular disease that has a
   multifactorial etiology, with oxidative stress as an important
   component. Our previous observation of a significant diabetes-related
   increase in rat cardiac catalase (CAT) activity suggested that CAT could
   play a major role in delaying the development of diabetic
   cardiomyopathy. Thus, in the present work, we examined the effects of
   the daily administration of the CAT inhibitor, 3-amino-1,2,4-triazole (1
   mg/g), on the hearts of streptozotocin (STZ)-induced diabetic rats.
   Administration of CAT inhibitor was started from the 15th day after the
   last STZ treatment (40 mg/kg/5 days), and maintained until the end of
   the 4th or 6th weeks of diabetes. Compared to untreated diabetic rats,
   at the end of the observation period, CAT inhibition lowered the induced
   level of cardiac CAT activity to the basal level and decreased CAT
   protein expression, mediated through a decline in the nuclear factor
   erythroid-derived 2-like 2 /nuclear factor-kappa B p65 (Nrf2/NF-kappa B
   p65) subunit ratio. The perturbed antioxidant defenses resulting from
   CAT inhibition promoted increased H2O2 production (P < 0.05) and lipid
   peroxidation (P < 0.05). Generated cytotoxic stimuli increased DNA
   damage (P < 0.05) and activated pro-apoptotic events, observed as a
   decrease (P < 0.05) in the ratio of the apoptosis regulator proteins
   Bcl-2/Bax, increased (P < 0.05) presence of the poly(ADP-ribose)
   polymerase-1 (PARP-1) 85 kDa apoptotic fragment and cytoplasmic levels
   of cytochrome C. These findings confirm an important function of CAT in
   the suppression of events leading to diabetes-promoted cardiac
   dysfunction and cardiomyopathy.",
journal = "Journal of Physiology and Biochemistry",
title = "Catalase inhibition in diabetic rats potentiates DNA damage and
 apoptotic cell death setting the stage for cardiomyopathy",
number = "4",
volume = "70",
doi = "10.1007/s13105-014-0363-y",
pages = "947-959"
}

Ivanović Matić, S., Bogojević, D., Martinović, V., Petrovic, A., Jovanovic-Stojanov, S., Poznanović, G.,& Grigorov, I.. (2014). Catalase inhibition in diabetic rats potentiates DNA damage and
 apoptotic cell death setting the stage for cardiomyopathy. in Journal of Physiology and Biochemistry, 70(4), 947-959.
https://doi.org/10.1007/s13105-014-0363-y

Ivanović Matić S, Bogojević D, Martinović V, Petrovic A, Jovanovic-Stojanov S, Poznanović G, Grigorov I. Catalase inhibition in diabetic rats potentiates DNA damage and
 apoptotic cell death setting the stage for cardiomyopathy. in Journal of Physiology and Biochemistry. 2014;70(4):947-959.
doi:10.1007/s13105-014-0363-y .

Ivanović Matić, Svetlana, Bogojević, Desanka, Martinović, Vesna, Petrovic, Anja, Jovanovic-Stojanov, Sofija, Poznanović, Goran, Grigorov, Ilijana, "Catalase inhibition in diabetic rats potentiates DNA damage and
 apoptotic cell death setting the stage for cardiomyopathy" in Journal of Physiology and Biochemistry, 70, no. 4 (2014):947-959,
https://doi.org/10.1007/s13105-014-0363-y . .

TY  - CONF
AU  - Matić, Sanja
AU  - Stanić, Snežana
AU  - Bogojević, Desanka
AU  - Solujić, Slavica
AU  - Mladenović, Milan
AU  - Stanković, Nevena
AU  - Mihailović, Vladimir
AU  - Katanić, Jelena
AU  - Mihailović, Mirjana
PY  - 2013
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6141
AB  - The plant Cotinus coggygria Scop. (family Anacardiaceae) is commonly used in folk medicine for the treat­ment of various illnesses, such as diarrhea, paradontosis, gastric and duodenal ulcers. Different parts of this plant have been subjected to pharmacological evaluation for their potential antihaemorragic, wound-healing, anti­inflammatory, and antimicrobial activity. The present study was undertaken to investigate the phenolic conten according to the Folin-Ciocalteu procedure, while the spectrophotometric method with aluminium chloride was used for the determination of total ftavonoids. The phenolic and flavonoid composition of extract were deter­mined by the HPLC method. Antioxidant activiy was quantitatively determined using a DPPH radical scaveng­ing assay. To examine the antigenotoxic potential using the comet assay, Wistar rats were treated with 100 mg/ kg body weight of pyrogallol, which possesses a potent ability to generate free radicals and induce oxidative stress. The content of total phenols and ftavonoids was 3.78 mg of gallic acid/g of dry plant material and 8.29 mg of rutin/g of dry plant material, respectively. HPLC analysis showed that myricetin was the dominant compound (511.5 µg/g), while hydroxyl derivatives of cinnammic acids (chlorogenic, caffeic, coumaric, ferulic and rosmaric acid) were identified in the extract in varying amount. The neutralisation of DPPH radicals was up to 95%, while the maximum inhibition concentration is approximately 125 µg/ml. The dose of 500 mg/kg body weight of the extract, that display no genotoxic activity, and its main flavonoid compound myricetin, in equivalent amount as present in the extract, were applied intraperitoneally either 2 or 12 h prior to pyrogallol. As measured by the decrease in total score and tail moment, the DNA damage in liver was reduced by the extract and myricetin.
PB  - Belgrade: Serbian Plant Physiology Society
C3  - Programme and Abstracts: 1st International Conference on Plant Biology and 20th Symposium of the Serbian Plant Physiology Society; 2013 Jun 4-7; Subotica, Serbia
T1  - Chemical composition, antioxidant and antigenotoxic activities of Cotinus coggygria stem extract
SP  - 90
EP  - 91
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_6141
ER  - 

@conference{
author = "Matić, Sanja and Stanić, Snežana and Bogojević, Desanka and Solujić, Slavica and Mladenović, Milan and Stanković, Nevena and Mihailović, Vladimir and Katanić, Jelena and Mihailović, Mirjana",
year = "2013",
abstract = "The plant Cotinus coggygria Scop. (family Anacardiaceae) is commonly used in folk medicine for the treat­ment of various illnesses, such as diarrhea, paradontosis, gastric and duodenal ulcers. Different parts of this plant have been subjected to pharmacological evaluation for their potential antihaemorragic, wound-healing, anti­inflammatory, and antimicrobial activity. The present study was undertaken to investigate the phenolic conten according to the Folin-Ciocalteu procedure, while the spectrophotometric method with aluminium chloride was used for the determination of total ftavonoids. The phenolic and flavonoid composition of extract were deter­mined by the HPLC method. Antioxidant activiy was quantitatively determined using a DPPH radical scaveng­ing assay. To examine the antigenotoxic potential using the comet assay, Wistar rats were treated with 100 mg/ kg body weight of pyrogallol, which possesses a potent ability to generate free radicals and induce oxidative stress. The content of total phenols and ftavonoids was 3.78 mg of gallic acid/g of dry plant material and 8.29 mg of rutin/g of dry plant material, respectively. HPLC analysis showed that myricetin was the dominant compound (511.5 µg/g), while hydroxyl derivatives of cinnammic acids (chlorogenic, caffeic, coumaric, ferulic and rosmaric acid) were identified in the extract in varying amount. The neutralisation of DPPH radicals was up to 95%, while the maximum inhibition concentration is approximately 125 µg/ml. The dose of 500 mg/kg body weight of the extract, that display no genotoxic activity, and its main flavonoid compound myricetin, in equivalent amount as present in the extract, were applied intraperitoneally either 2 or 12 h prior to pyrogallol. As measured by the decrease in total score and tail moment, the DNA damage in liver was reduced by the extract and myricetin.",
publisher = "Belgrade: Serbian Plant Physiology Society",
journal = "Programme and Abstracts: 1st International Conference on Plant Biology and 20th Symposium of the Serbian Plant Physiology Society; 2013 Jun 4-7; Subotica, Serbia",
title = "Chemical composition, antioxidant and antigenotoxic activities of Cotinus coggygria stem extract",
pages = "90-91",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_6141"
}

Matić, S., Stanić, S., Bogojević, D., Solujić, S., Mladenović, M., Stanković, N., Mihailović, V., Katanić, J.,& Mihailović, M.. (2013). Chemical composition, antioxidant and antigenotoxic activities of Cotinus coggygria stem extract. in Programme and Abstracts: 1st International Conference on Plant Biology and 20th Symposium of the Serbian Plant Physiology Society; 2013 Jun 4-7; Subotica, Serbia
Belgrade: Serbian Plant Physiology Society., 90-91.
https://hdl.handle.net/21.15107/rcub_ibiss_6141

Matić S, Stanić S, Bogojević D, Solujić S, Mladenović M, Stanković N, Mihailović V, Katanić J, Mihailović M. Chemical composition, antioxidant and antigenotoxic activities of Cotinus coggygria stem extract. in Programme and Abstracts: 1st International Conference on Plant Biology and 20th Symposium of the Serbian Plant Physiology Society; 2013 Jun 4-7; Subotica, Serbia. 2013;:90-91.
https://hdl.handle.net/21.15107/rcub_ibiss_6141 .

Matić, Sanja, Stanić, Snežana, Bogojević, Desanka, Solujić, Slavica, Mladenović, Milan, Stanković, Nevena, Mihailović, Vladimir, Katanić, Jelena, Mihailović, Mirjana, "Chemical composition, antioxidant and antigenotoxic activities of Cotinus coggygria stem extract" in Programme and Abstracts: 1st International Conference on Plant Biology and 20th Symposium of the Serbian Plant Physiology Society; 2013 Jun 4-7; Subotica, Serbia (2013):90-91,
https://hdl.handle.net/21.15107/rcub_ibiss_6141 .

TY  - CONF
AU  - Petrović, Anja
AU  - Martinović, Vesna
AU  - Bogojević, Desanka
AU  - Jovanović Stojanov, Sofija
AU  - Ivanović-Matić, Svetlana
AU  - Poznanović, Goran
AU  - Grigorov, Ilijana
PY  - 2013
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5430
AB  - Dijabetes predstavlja metabolički poremećaj koji je okarakterisan hiperglikemijom i sa njom udruženim oksidativnim stresom koji dovodi do oštećenja i disfunkcije mnogih organa. Patološke promene morfologije i funkcije jetre tokom razvoja dijabetesa glavni su uzroci različitih bolesti jetre. Kod dijabetičnih pacijenata dolazi do promena u veličini jetre kao rezultat izmenjenog broja ćelija usled njihovog rasta ili ćelijske smrti. U osnovi üelijske smrti putem nekroze nalaze se DNK oštećenja. Obzirom da tokom dijabetesa dolazi do smanjenja nivoa melatonina, u ovom radu ispitivan je antioksidativni uticaj dnevnog unosa melatonina na stepen DNK oštećenja i prisustvo nekrotskih promena u ćelijama jetre pacova kod kojih je dijabetes izazvan jednokratnim injeciranjem streptozotocina u dozi od 65 mg/kg. Eksperiment su činile kontrolna grupa pacova soja Wistar, grupa koja je primala melatonin (0.2 mg/kg), grupa sa dijabetesom i grupa dijabetičnih pacova tretiranih melatoninom. Tretman melatoninom počeo je tri dana pre injeciranja streptozotocina i trajao je četiri nedelje. Stepen oksidativnog stresa praćen je određivanjem lipidnog statusa i merenjem koncentracije vodonik peroksida (H2O2) u cirkulaciji i jetri. Oštećenje jetre je utvrđivano histološki i preko serumskog nivoa alanin aminotransferaze, aspartat aminotransferaze i alkalne fosfataze. Oštećenja DNK ispitivana su Komet analizom. Prisustvo nekrotskih promena praćeno je histološki i imunoblot analizom profila sečenja DNK reparacionog enzima, PARP-1 (engl. Poly(ADP-ribose)polymerase-1) i subćelijske lokalizacije i ekstraćelijskog prisustva signalnog proteina nekroze, HMGB1 (engl. High Mobility Group Box 1). Dijabetični pacovi tretirani melatoninom ispoljavali su značajno niži nivo oksidativnog stresa i oštećenja jetre u odnosu na dijabetične. Melatonin je očuvao strukturu jetre dijabetičnih pacova i značajno smanjio nivo hidropsne degeneracije i broj nekrotičnih ćelija što korelira sa smanjenjem DNK oštećenja za 77%, redukovanom pojavom nekrotskih fragmenata PARP-1 (55kDa i 62 kDa) i zadržavanjem HMGB1 proteina u jedru. Zaključeno je da melatonin svojim antioksidativnim delovanjem štiti jetru od oštećenja uzrokovanih dijabetičnim stanjem i da bi mogao biti od koristi kao vid terapije kod obolelih od dijabetesa.
PB  - Beograd: Srpsko društvo za mitohondrijalnu i slobodno-radikalsku fiziologiju
PB  - Beograd: Ministarstvo prosvete, nauke i tehnološkog razvoja
PB  - Beograd: Biološki fakultet
PB  - Niš: Medicinski fakultet
C3  - Knjiga sažetaka: Drugi kongres Život sa slobodnim radikalima: Hemija, Biologija, Medicina, SDMSRF-2013; 2013 Sep 28; Niš, Serbia
T1  - Antinekrotski efekat melatonina u jetri dijabetičnih pacova
SP  - 35
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5430
ER  - 

@conference{
author = "Petrović, Anja and Martinović, Vesna and Bogojević, Desanka and Jovanović Stojanov, Sofija and Ivanović-Matić, Svetlana and Poznanović, Goran and Grigorov, Ilijana",
year = "2013",
abstract = "Dijabetes predstavlja metabolički poremećaj koji je okarakterisan hiperglikemijom i sa njom udruženim oksidativnim stresom koji dovodi do oštećenja i disfunkcije mnogih organa. Patološke promene morfologije i funkcije jetre tokom razvoja dijabetesa glavni su uzroci različitih bolesti jetre. Kod dijabetičnih pacijenata dolazi do promena u veličini jetre kao rezultat izmenjenog broja ćelija usled njihovog rasta ili ćelijske smrti. U osnovi üelijske smrti putem nekroze nalaze se DNK oštećenja. Obzirom da tokom dijabetesa dolazi do smanjenja nivoa melatonina, u ovom radu ispitivan je antioksidativni uticaj dnevnog unosa melatonina na stepen DNK oštećenja i prisustvo nekrotskih promena u ćelijama jetre pacova kod kojih je dijabetes izazvan jednokratnim injeciranjem streptozotocina u dozi od 65 mg/kg. Eksperiment su činile kontrolna grupa pacova soja Wistar, grupa koja je primala melatonin (0.2 mg/kg), grupa sa dijabetesom i grupa dijabetičnih pacova tretiranih melatoninom. Tretman melatoninom počeo je tri dana pre injeciranja streptozotocina i trajao je četiri nedelje. Stepen oksidativnog stresa praćen je određivanjem lipidnog statusa i merenjem koncentracije vodonik peroksida (H2O2) u cirkulaciji i jetri. Oštećenje jetre je utvrđivano histološki i preko serumskog nivoa alanin aminotransferaze, aspartat aminotransferaze i alkalne fosfataze. Oštećenja DNK ispitivana su Komet analizom. Prisustvo nekrotskih promena praćeno je histološki i imunoblot analizom profila sečenja DNK reparacionog enzima, PARP-1 (engl. Poly(ADP-ribose)polymerase-1) i subćelijske lokalizacije i ekstraćelijskog prisustva signalnog proteina nekroze, HMGB1 (engl. High Mobility Group Box 1). Dijabetični pacovi tretirani melatoninom ispoljavali su značajno niži nivo oksidativnog stresa i oštećenja jetre u odnosu na dijabetične. Melatonin je očuvao strukturu jetre dijabetičnih pacova i značajno smanjio nivo hidropsne degeneracije i broj nekrotičnih ćelija što korelira sa smanjenjem DNK oštećenja za 77%, redukovanom pojavom nekrotskih fragmenata PARP-1 (55kDa i 62 kDa) i zadržavanjem HMGB1 proteina u jedru. Zaključeno je da melatonin svojim antioksidativnim delovanjem štiti jetru od oštećenja uzrokovanih dijabetičnim stanjem i da bi mogao biti od koristi kao vid terapije kod obolelih od dijabetesa.",
publisher = "Beograd: Srpsko društvo za mitohondrijalnu i slobodno-radikalsku fiziologiju, Beograd: Ministarstvo prosvete, nauke i tehnološkog razvoja, Beograd: Biološki fakultet, Niš: Medicinski fakultet",
journal = "Knjiga sažetaka: Drugi kongres Život sa slobodnim radikalima: Hemija, Biologija, Medicina, SDMSRF-2013; 2013 Sep 28; Niš, Serbia",
title = "Antinekrotski efekat melatonina u jetri dijabetičnih pacova",
pages = "35",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5430"
}

Petrović, A., Martinović, V., Bogojević, D., Jovanović Stojanov, S., Ivanović-Matić, S., Poznanović, G.,& Grigorov, I.. (2013). Antinekrotski efekat melatonina u jetri dijabetičnih pacova. in Knjiga sažetaka: Drugi kongres Život sa slobodnim radikalima: Hemija, Biologija, Medicina, SDMSRF-2013; 2013 Sep 28; Niš, Serbia
Beograd: Srpsko društvo za mitohondrijalnu i slobodno-radikalsku fiziologiju., 35.
https://hdl.handle.net/21.15107/rcub_ibiss_5430

Petrović A, Martinović V, Bogojević D, Jovanović Stojanov S, Ivanović-Matić S, Poznanović G, Grigorov I. Antinekrotski efekat melatonina u jetri dijabetičnih pacova. in Knjiga sažetaka: Drugi kongres Život sa slobodnim radikalima: Hemija, Biologija, Medicina, SDMSRF-2013; 2013 Sep 28; Niš, Serbia. 2013;:35.
https://hdl.handle.net/21.15107/rcub_ibiss_5430 .

Petrović, Anja, Martinović, Vesna, Bogojević, Desanka, Jovanović Stojanov, Sofija, Ivanović-Matić, Svetlana, Poznanović, Goran, Grigorov, Ilijana, "Antinekrotski efekat melatonina u jetri dijabetičnih pacova" in Knjiga sažetaka: Drugi kongres Život sa slobodnim radikalima: Hemija, Biologija, Medicina, SDMSRF-2013; 2013 Sep 28; Niš, Serbia (2013):35,
https://hdl.handle.net/21.15107/rcub_ibiss_5430 .

TY  - JOUR
AU  - Matić, Sanja
AU  - Stanić, Snežana
AU  - Bogojević, Desanka
AU  - Vidaković, Melita
AU  - Grdović, Nevena
AU  - Dinić, Svetlana
AU  - Solujić, Slavica
AU  - Mladenović, Milan
AU  - Stanković, Nevena
AU  - Mihailović, Mirjana
PY  - 2013
UR  - http://www.sciencedirect.com/science/article/pii/S1383571813001836
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3188
AB  - The present study was undertaken to investigate the hepatoprotective effect of the methanol extract of Cotinus coggygria Scop. in rats exposed to the hepatotoxic compound pyrogallol. Assessed with the alkaline version of the comet assay, 1000 and 2000. mg/kg body weight (bw) of the extract showed a low level of genotoxicity, while 500. mg/kg bw of the extract showed no genotoxic potential. Quantitative HPLC analysis of phenolic acids and flavonoids in the methanol extract of C. coggygria showed that myricetin was a major component. To test the hepatoprotective effect, a non-genotoxic dose of the C. coggygria extract and an equivalent amount of synthetic myricetin, as present in the extract, were applied either 2 or 12. h prior to administration of 100. mg/kg bw of pyrogallol. The extract and myricetin promoted restoration of hepatic function by significantly reducing pyrogallol-induced elevation in the serum enzymes AST, ALT, ALP and in total bilirubin. As measured by the decrease in total score and tail moment, the DNA damage in liver was also reduced by the extract and by myricetin. Our results suggest that pro-surviving Akt activity and STAT3 protein expression play important roles in decreasing DNA damage and in mediating hepatic protection by the extract. These results suggest that myricetin, as a major component in the extract, is responsible for the antigenotoxic and hepatoprotective properties of the methanol extract of C. coggygria against pyrogallol-induced toxicity. © 2013 Elsevier B.V.
PB  - Elsevier
T2  - Mutation Research - Genetic Toxicology and Environmental Mutagenesis
T2  - Mutation Research - Genetic Toxicology and Environmental Mutagenesis
T1  - Methanol extract from the stem of Cotinus coggygria Scop., and its major bioactive phytochemical constituent myricetin modulate pyrogallol-induced DNA damage and liver injury
IS  - 2
VL  - 755
DO  - 10.1016/j.mrgentox.2013.03.011
SP  - 81
EP  - 89
ER  - 

@article{
author = "Matić, Sanja and Stanić, Snežana and Bogojević, Desanka and Vidaković, Melita and Grdović, Nevena and Dinić, Svetlana and Solujić, Slavica and Mladenović, Milan and Stanković, Nevena and Mihailović, Mirjana",
year = "2013",
abstract = "The present study was undertaken to investigate the hepatoprotective effect of the methanol extract of Cotinus coggygria Scop. in rats exposed to the hepatotoxic compound pyrogallol. Assessed with the alkaline version of the comet assay, 1000 and 2000. mg/kg body weight (bw) of the extract showed a low level of genotoxicity, while 500. mg/kg bw of the extract showed no genotoxic potential. Quantitative HPLC analysis of phenolic acids and flavonoids in the methanol extract of C. coggygria showed that myricetin was a major component. To test the hepatoprotective effect, a non-genotoxic dose of the C. coggygria extract and an equivalent amount of synthetic myricetin, as present in the extract, were applied either 2 or 12. h prior to administration of 100. mg/kg bw of pyrogallol. The extract and myricetin promoted restoration of hepatic function by significantly reducing pyrogallol-induced elevation in the serum enzymes AST, ALT, ALP and in total bilirubin. As measured by the decrease in total score and tail moment, the DNA damage in liver was also reduced by the extract and by myricetin. Our results suggest that pro-surviving Akt activity and STAT3 protein expression play important roles in decreasing DNA damage and in mediating hepatic protection by the extract. These results suggest that myricetin, as a major component in the extract, is responsible for the antigenotoxic and hepatoprotective properties of the methanol extract of C. coggygria against pyrogallol-induced toxicity. © 2013 Elsevier B.V.",
publisher = "Elsevier",
journal = "Mutation Research - Genetic Toxicology and Environmental Mutagenesis, Mutation Research - Genetic Toxicology and Environmental Mutagenesis",
title = "Methanol extract from the stem of Cotinus coggygria Scop., and its major bioactive phytochemical constituent myricetin modulate pyrogallol-induced DNA damage and liver injury",
number = "2",
volume = "755",
doi = "10.1016/j.mrgentox.2013.03.011",
pages = "81-89"
}

Matić, S., Stanić, S., Bogojević, D., Vidaković, M., Grdović, N., Dinić, S., Solujić, S., Mladenović, M., Stanković, N.,& Mihailović, M.. (2013). Methanol extract from the stem of Cotinus coggygria Scop., and its major bioactive phytochemical constituent myricetin modulate pyrogallol-induced DNA damage and liver injury. in Mutation Research - Genetic Toxicology and Environmental Mutagenesis
Elsevier., 755(2), 81-89.
https://doi.org/10.1016/j.mrgentox.2013.03.011

Matić S, Stanić S, Bogojević D, Vidaković M, Grdović N, Dinić S, Solujić S, Mladenović M, Stanković N, Mihailović M. Methanol extract from the stem of Cotinus coggygria Scop., and its major bioactive phytochemical constituent myricetin modulate pyrogallol-induced DNA damage and liver injury. in Mutation Research - Genetic Toxicology and Environmental Mutagenesis. 2013;755(2):81-89.
doi:10.1016/j.mrgentox.2013.03.011 .

Matić, Sanja, Stanić, Snežana, Bogojević, Desanka, Vidaković, Melita, Grdović, Nevena, Dinić, Svetlana, Solujić, Slavica, Mladenović, Milan, Stanković, Nevena, Mihailović, Mirjana, "Methanol extract from the stem of Cotinus coggygria Scop., and its major bioactive phytochemical constituent myricetin modulate pyrogallol-induced DNA damage and liver injury" in Mutation Research - Genetic Toxicology and Environmental Mutagenesis, 755, no. 2 (2013):81-89,
https://doi.org/10.1016/j.mrgentox.2013.03.011 . .

TY  - JOUR
AU  - Arambašić Jovanović, Jelena
AU  - Mihailović, Mirjana
AU  - Bogojević, Desanka
AU  - Ivanović Matić, Svetlana
AU  - Uskoković, Aleksandra
AU  - Poznanović, Goran
AU  - Grigorov, Ilijana
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1040
AB  - Haptoglobin is a hemoglobin-binding acute-phase protein which possesses anti-inflammatory and antioxidative properties. In this study, we investigated changes in protein expression of rat haptoglobin under diabetes-related inflammatory and oxidative stress conditions induced by an i.p. injection of streptozotocin. The progress of diabetes during an 8-week follow-up period was associated with the increased presence of haptoglobin in the serum and in the liver. This increase was most prominent during the first 2 weeks after which it started to decline. Temporary changes in haptoglobin expression strongly correlated with the serum levels of TNF-alpha and IL-6. Lower haptoglobin expression at the fourth week and thereafter correlated with a decrease in TNF-alpha concentration and changes in the TNF-alpha/IL-6 ratio. Based on the decrease of GSH/GSSG ratio and antioxidant enzyme activities in the liver until the end of fourth week, it was concluded that the liver was exposed to oxidative stress and injury which in the presence of the abovementioned inflammatory mediators lead to different haptoglobin expression profiles at different stages of diabetes. An inverse correlation was observed between the haptoglobin and free iron serum levels in diabetic rats. The higher levels of haptoglobin during the first 2 weeks were accompanied by a lower level of free iron. In view of the established function of haptoglobin, we discuss its possible role in decreasing oxidative stress during the early stage of diabetes.
PB  - Springer Nature
T2  - Journal of Physiology and Biochemistry
T1  - Haptoglobin and the inflammatory and oxidative status in experimental diabetic rats: antioxidant role of haptoglobin
IS  - 1
VL  - 69
DO  - 10.1007/s13105-012-0186-7
SP  - 45
EP  - 58
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1040
ER  - 

@article{
author = "Arambašić Jovanović, Jelena and Mihailović, Mirjana and Bogojević, Desanka and Ivanović Matić, Svetlana and Uskoković, Aleksandra and Poznanović, Goran and Grigorov, Ilijana",
year = "2013",
abstract = "Haptoglobin is a hemoglobin-binding acute-phase protein which possesses anti-inflammatory and antioxidative properties. In this study, we investigated changes in protein expression of rat haptoglobin under diabetes-related inflammatory and oxidative stress conditions induced by an i.p. injection of streptozotocin. The progress of diabetes during an 8-week follow-up period was associated with the increased presence of haptoglobin in the serum and in the liver. This increase was most prominent during the first 2 weeks after which it started to decline. Temporary changes in haptoglobin expression strongly correlated with the serum levels of TNF-alpha and IL-6. Lower haptoglobin expression at the fourth week and thereafter correlated with a decrease in TNF-alpha concentration and changes in the TNF-alpha/IL-6 ratio. Based on the decrease of GSH/GSSG ratio and antioxidant enzyme activities in the liver until the end of fourth week, it was concluded that the liver was exposed to oxidative stress and injury which in the presence of the abovementioned inflammatory mediators lead to different haptoglobin expression profiles at different stages of diabetes. An inverse correlation was observed between the haptoglobin and free iron serum levels in diabetic rats. The higher levels of haptoglobin during the first 2 weeks were accompanied by a lower level of free iron. In view of the established function of haptoglobin, we discuss its possible role in decreasing oxidative stress during the early stage of diabetes.",
publisher = "Springer Nature",
journal = "Journal of Physiology and Biochemistry",
title = "Haptoglobin and the inflammatory and oxidative status in experimental diabetic rats: antioxidant role of haptoglobin",
number = "1",
volume = "69",
doi = "10.1007/s13105-012-0186-7",
pages = "45-58",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1040"
}

Arambašić Jovanović, J., Mihailović, M., Bogojević, D., Ivanović Matić, S., Uskoković, A., Poznanović, G.,& Grigorov, I.. (2013). Haptoglobin and the inflammatory and oxidative status in experimental diabetic rats: antioxidant role of haptoglobin. in Journal of Physiology and Biochemistry
Springer Nature., 69(1), 45-58.
https://doi.org/10.1007/s13105-012-0186-7
https://hdl.handle.net/21.15107/rcub_ibiss_1040

Arambašić Jovanović J, Mihailović M, Bogojević D, Ivanović Matić S, Uskoković A, Poznanović G, Grigorov I. Haptoglobin and the inflammatory and oxidative status in experimental diabetic rats: antioxidant role of haptoglobin. in Journal of Physiology and Biochemistry. 2013;69(1):45-58.
doi:10.1007/s13105-012-0186-7
https://hdl.handle.net/21.15107/rcub_ibiss_1040 .

Arambašić Jovanović, Jelena, Mihailović, Mirjana, Bogojević, Desanka, Ivanović Matić, Svetlana, Uskoković, Aleksandra, Poznanović, Goran, Grigorov, Ilijana, "Haptoglobin and the inflammatory and oxidative status in experimental diabetic rats: antioxidant role of haptoglobin" in Journal of Physiology and Biochemistry, 69, no. 1 (2013):45-58,
https://doi.org/10.1007/s13105-012-0186-7 .,
https://hdl.handle.net/21.15107/rcub_ibiss_1040 .

TY  - CONF
AU  - Petrović, Anja
AU  - Ivanović-Matić, Svetlana
AU  - Bogojević, Desanka
AU  - Martinović, Vesna
AU  - Jovanović-Stojanov, Sofija
AU  - Poznanović, Goran
AU  - Grigorov, Ilijana
PY  - 2013
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5651
AB  - Oxidative stress-related cardiomyocyte damage in diabetes represents a major risk factor for heart disease. Reactive oxygen species triggers a series of deleterious stimuli that result in protein and DNA damage, cell dysfunction and cell death. Our previous study showed that the absence of cardiomyopathy in rats with streptozotocin (STZ)-induced diabetes is accompanied with significantly higher antioxidative activity of catalase (CAT), suggesting that CAT may be one of the key enzymes in heart protection during diabetes. To confirm this hypothesis we analysed oxidative status and extent of DNA damage in cardiomyocytes of diabetic rats with inhibited CAT activity. Diabetes was induced by intraperitoneal (i.p.) injection of ST2 at 40 mg/kg/day for five consecutive days. Inhibition of CAT activity was established by daily i.p. administration of 1 mg/kg 3-amino-1,2,4 triazole throughout the 4 week period, starting from the 15th day of STZ administration. Increased lipid per-oxidation and H2O2, concentration in the heart of diabetic rats with inhibited CAT activity indicated higher level of oxidative stress when compared with diabetic ones. This is followed with decline of glutathione level, activity of glutathione peroxidase and total superoxide dismutase and increased activity of manganese superoxide dismutase whose overexpression could potentiate cardiac CAT activity. According to comet assay, impairment in antioxidant defense system led to significantly increased DNA damage in cardiomyocytes of rats with inhibited CAT activity in comparison with cardiomyocytes of diabetic rats. Also, Western immunoblot revealed that inhibition of CAT activity in diabetic heart was followed by twofold decrease in CAT expression as a result of the decrease in expression of Nrf2, the main transcription factor involved in CAT gene induction. These results suggest that. CAT expression and activity is crucial in prevention of heart damage during diabetes.
PB  - Heidelberg, Germany: EMBL
C3  - Abstracts presented at the 15th international EMBL PhD Symposium: Competition in Biology: The race for survival from molecules to systems; 2013 Nov 21-23; Heidelberg, Germany
T1  - Catalase prevents cardiomyocyte DNA damage during diabetes
SP  - 55
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5651
ER  - 

@conference{
author = "Petrović, Anja and Ivanović-Matić, Svetlana and Bogojević, Desanka and Martinović, Vesna and Jovanović-Stojanov, Sofija and Poznanović, Goran and Grigorov, Ilijana",
year = "2013",
abstract = "Oxidative stress-related cardiomyocyte damage in diabetes represents a major risk factor for heart disease. Reactive oxygen species triggers a series of deleterious stimuli that result in protein and DNA damage, cell dysfunction and cell death. Our previous study showed that the absence of cardiomyopathy in rats with streptozotocin (STZ)-induced diabetes is accompanied with significantly higher antioxidative activity of catalase (CAT), suggesting that CAT may be one of the key enzymes in heart protection during diabetes. To confirm this hypothesis we analysed oxidative status and extent of DNA damage in cardiomyocytes of diabetic rats with inhibited CAT activity. Diabetes was induced by intraperitoneal (i.p.) injection of ST2 at 40 mg/kg/day for five consecutive days. Inhibition of CAT activity was established by daily i.p. administration of 1 mg/kg 3-amino-1,2,4 triazole throughout the 4 week period, starting from the 15th day of STZ administration. Increased lipid per-oxidation and H2O2, concentration in the heart of diabetic rats with inhibited CAT activity indicated higher level of oxidative stress when compared with diabetic ones. This is followed with decline of glutathione level, activity of glutathione peroxidase and total superoxide dismutase and increased activity of manganese superoxide dismutase whose overexpression could potentiate cardiac CAT activity. According to comet assay, impairment in antioxidant defense system led to significantly increased DNA damage in cardiomyocytes of rats with inhibited CAT activity in comparison with cardiomyocytes of diabetic rats. Also, Western immunoblot revealed that inhibition of CAT activity in diabetic heart was followed by twofold decrease in CAT expression as a result of the decrease in expression of Nrf2, the main transcription factor involved in CAT gene induction. These results suggest that. CAT expression and activity is crucial in prevention of heart damage during diabetes.",
publisher = "Heidelberg, Germany: EMBL",
journal = "Abstracts presented at the 15th international EMBL PhD Symposium: Competition in Biology: The race for survival from molecules to systems; 2013 Nov 21-23; Heidelberg, Germany",
title = "Catalase prevents cardiomyocyte DNA damage during diabetes",
pages = "55",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5651"
}

Petrović, A., Ivanović-Matić, S., Bogojević, D., Martinović, V., Jovanović-Stojanov, S., Poznanović, G.,& Grigorov, I.. (2013). Catalase prevents cardiomyocyte DNA damage during diabetes. in Abstracts presented at the 15th international EMBL PhD Symposium: Competition in Biology: The race for survival from molecules to systems; 2013 Nov 21-23; Heidelberg, Germany
Heidelberg, Germany: EMBL., 55.
https://hdl.handle.net/21.15107/rcub_ibiss_5651

Petrović A, Ivanović-Matić S, Bogojević D, Martinović V, Jovanović-Stojanov S, Poznanović G, Grigorov I. Catalase prevents cardiomyocyte DNA damage during diabetes. in Abstracts presented at the 15th international EMBL PhD Symposium: Competition in Biology: The race for survival from molecules to systems; 2013 Nov 21-23; Heidelberg, Germany. 2013;:55.
https://hdl.handle.net/21.15107/rcub_ibiss_5651 .

Petrović, Anja, Ivanović-Matić, Svetlana, Bogojević, Desanka, Martinović, Vesna, Jovanović-Stojanov, Sofija, Poznanović, Goran, Grigorov, Ilijana, "Catalase prevents cardiomyocyte DNA damage during diabetes" in Abstracts presented at the 15th international EMBL PhD Symposium: Competition in Biology: The race for survival from molecules to systems; 2013 Nov 21-23; Heidelberg, Germany (2013):55,
https://hdl.handle.net/21.15107/rcub_ibiss_5651 .

TY  - CONF
AU  - Jovanović Stojanov, Sofija
AU  - Martinović, Vesna
AU  - Bogojević, Desanka
AU  - Ivanović-Matić, Svetlana
AU  - Petrović, Anja
AU  - Poznanović, Goran
AU  - Grigorov, Ilijana
PY  - 2013
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5429
AB  - Hipoinsulinemija i hiperglikemija koje nastaju tokom dijabetesa, uzrokuju pojavu metaboličkog i oksidativnog stresa koji dovode do stanja hronične inflamacije, progresivne disfunkcije i oštećenja jetre. Za predikciju i prevenciju pojave dijabetičnih komplikacija u jetri od interesa je identifikacija endogenih molekula koji svojim delovanjem doprinose njenom oštećenju. U tom smislu izdvaja se protein HMGB1. Prvobitno okarakterisan kao DNK- vezujući protein sa ulogom u organizaciji hromatinske strukture, HMGB1 može biti prisutan u ekstraćelijskom miljeu gde ima ulogu proinflamatornog citokina i medijatora tkivnih oštećenja. U vanćelijsku sredinu HMGB1 dospeva pasivno iz nekroznih ili oštećenih ćelija ili regulisanom sekrecijom iz ćelija izloženih stresu. U ovom radu ispitivan je uticaj oksidativnog statusa na subćelijsku lokalizaciju i ukupno prisustvo HMGB1 proteina u jetri i serumu pacova sa dijabetesom tipa I i promene nastale nakon tretmana dijabetičnih pacova sa antioksidansom melatoninom.
Dijabetes tipa I uspostavljen je davanjem jednokratne doze streptozotocina (65 mg/kg) pacovima soja Wistar. Tretman kontrolnih i dijabetičnih pacova melatoninom (0.2 mg/kg) započet je tri dana pre indukcije dijabetesa i vršen je svakodnevno tokom 4   nedelje.
Dijabetično stanje karakteriše značajan porast koncentracije vodonik peroksida (H2O2), i superoksid anjon radikala (O .-) u serumu, porast lipidne peroksidacije i pad aktivnosti antioksidativnih enzima katalaze, superoksid dismutaza i glutation S transferaze u serumu i
jetri. Ovakav oksidativni status prati značajni porast koncentracije alanin aminotransferaze (ALT), pokazatelja oštećenja jetre, za oko 3.2 puta kao i značajan porast nivoa HMGB1 proteina (2.1 put) u serumu i ukupnim homogenatima jetre (2.3 puta). Imunohistohemijski utvrđena je prevashodno citoplazmatska lokalizacija HMGB1 proteina tokom dijabetesa. Bolji oksidativni status uspostavljen tretmanom sa melatoninom dovodi do smanjenja ošteüenja jetre što je praćeno značajnim smanjenjem nivoa HMGB1 proteina u serumu i jetri i njegovim zadržavanjem u jedru ćelija jetre.
Dobijeni rezultati ukazuju da prisustvo HMGB1 proteina u serumu korelira sa stepenom oksidativnog stresa i oštećenjem jetre što navodi na zaključak da HMGB1 protein može biti potencijalni prognostički indikator tkivnih oštećenja kao i meta terapeutskog delovanja kojim bi se menjala njegova lokalizovanost i aktivnost, a time i redukovala disfunkcija jetre tokom dijabetesa.
PB  - Beograd: Srpsko društvo za mitohondrijalnu i slobodno-radikalsku fiziologiju
PB  - Beograd: Ministarstvo prosvete, nauke i tehnološkog razvoja
PB  - Beograd: Biološki fakultet
PB  - Niš: Medicinski fakultet
C3  - Knjiga sažetaka: Drugi kongres Život sa slobodnim radikalima: Hemija, Biologija, Medicina, SDMSRF-2013; 2013 Sep 28; Niš, Serbia
T1  - HMGB1 kao indikator oštećenja jetre uzrokovanog oksidativnim stresom tokom dijabetesa
SP  - 79
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5429
ER  - 

@conference{
author = "Jovanović Stojanov, Sofija and Martinović, Vesna and Bogojević, Desanka and Ivanović-Matić, Svetlana and Petrović, Anja and Poznanović, Goran and Grigorov, Ilijana",
year = "2013",
abstract = "Hipoinsulinemija i hiperglikemija koje nastaju tokom dijabetesa, uzrokuju pojavu metaboličkog i oksidativnog stresa koji dovode do stanja hronične inflamacije, progresivne disfunkcije i oštećenja jetre. Za predikciju i prevenciju pojave dijabetičnih komplikacija u jetri od interesa je identifikacija endogenih molekula koji svojim delovanjem doprinose njenom oštećenju. U tom smislu izdvaja se protein HMGB1. Prvobitno okarakterisan kao DNK- vezujući protein sa ulogom u organizaciji hromatinske strukture, HMGB1 može biti prisutan u ekstraćelijskom miljeu gde ima ulogu proinflamatornog citokina i medijatora tkivnih oštećenja. U vanćelijsku sredinu HMGB1 dospeva pasivno iz nekroznih ili oštećenih ćelija ili regulisanom sekrecijom iz ćelija izloženih stresu. U ovom radu ispitivan je uticaj oksidativnog statusa na subćelijsku lokalizaciju i ukupno prisustvo HMGB1 proteina u jetri i serumu pacova sa dijabetesom tipa I i promene nastale nakon tretmana dijabetičnih pacova sa antioksidansom melatoninom.
Dijabetes tipa I uspostavljen je davanjem jednokratne doze streptozotocina (65 mg/kg) pacovima soja Wistar. Tretman kontrolnih i dijabetičnih pacova melatoninom (0.2 mg/kg) započet je tri dana pre indukcije dijabetesa i vršen je svakodnevno tokom 4   nedelje.
Dijabetično stanje karakteriše značajan porast koncentracije vodonik peroksida (H2O2), i superoksid anjon radikala (O .-) u serumu, porast lipidne peroksidacije i pad aktivnosti antioksidativnih enzima katalaze, superoksid dismutaza i glutation S transferaze u serumu i
jetri. Ovakav oksidativni status prati značajni porast koncentracije alanin aminotransferaze (ALT), pokazatelja oštećenja jetre, za oko 3.2 puta kao i značajan porast nivoa HMGB1 proteina (2.1 put) u serumu i ukupnim homogenatima jetre (2.3 puta). Imunohistohemijski utvrđena je prevashodno citoplazmatska lokalizacija HMGB1 proteina tokom dijabetesa. Bolji oksidativni status uspostavljen tretmanom sa melatoninom dovodi do smanjenja ošteüenja jetre što je praćeno značajnim smanjenjem nivoa HMGB1 proteina u serumu i jetri i njegovim zadržavanjem u jedru ćelija jetre.
Dobijeni rezultati ukazuju da prisustvo HMGB1 proteina u serumu korelira sa stepenom oksidativnog stresa i oštećenjem jetre što navodi na zaključak da HMGB1 protein može biti potencijalni prognostički indikator tkivnih oštećenja kao i meta terapeutskog delovanja kojim bi se menjala njegova lokalizovanost i aktivnost, a time i redukovala disfunkcija jetre tokom dijabetesa.",
publisher = "Beograd: Srpsko društvo za mitohondrijalnu i slobodno-radikalsku fiziologiju, Beograd: Ministarstvo prosvete, nauke i tehnološkog razvoja, Beograd: Biološki fakultet, Niš: Medicinski fakultet",
journal = "Knjiga sažetaka: Drugi kongres Život sa slobodnim radikalima: Hemija, Biologija, Medicina, SDMSRF-2013; 2013 Sep 28; Niš, Serbia",
title = "HMGB1 kao indikator oštećenja jetre uzrokovanog oksidativnim stresom tokom dijabetesa",
pages = "79",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5429"
}

Jovanović Stojanov, S., Martinović, V., Bogojević, D., Ivanović-Matić, S., Petrović, A., Poznanović, G.,& Grigorov, I.. (2013). HMGB1 kao indikator oštećenja jetre uzrokovanog oksidativnim stresom tokom dijabetesa. in Knjiga sažetaka: Drugi kongres Život sa slobodnim radikalima: Hemija, Biologija, Medicina, SDMSRF-2013; 2013 Sep 28; Niš, Serbia
Beograd: Srpsko društvo za mitohondrijalnu i slobodno-radikalsku fiziologiju., 79.
https://hdl.handle.net/21.15107/rcub_ibiss_5429

Jovanović Stojanov S, Martinović V, Bogojević D, Ivanović-Matić S, Petrović A, Poznanović G, Grigorov I. HMGB1 kao indikator oštećenja jetre uzrokovanog oksidativnim stresom tokom dijabetesa. in Knjiga sažetaka: Drugi kongres Život sa slobodnim radikalima: Hemija, Biologija, Medicina, SDMSRF-2013; 2013 Sep 28; Niš, Serbia. 2013;:79.
https://hdl.handle.net/21.15107/rcub_ibiss_5429 .

Jovanović Stojanov, Sofija, Martinović, Vesna, Bogojević, Desanka, Ivanović-Matić, Svetlana, Petrović, Anja, Poznanović, Goran, Grigorov, Ilijana, "HMGB1 kao indikator oštećenja jetre uzrokovanog oksidativnim stresom tokom dijabetesa" in Knjiga sažetaka: Drugi kongres Život sa slobodnim radikalima: Hemija, Biologija, Medicina, SDMSRF-2013; 2013 Sep 28; Niš, Serbia (2013):79,
https://hdl.handle.net/21.15107/rcub_ibiss_5429 .

TY  - JOUR
AU  - Martinović, Vesna
AU  - Grigorov, Ilijana
AU  - Bogojević, Desanka
AU  - Petrović, Anja
AU  - Jovanović Stojanov, Sofija
AU  - Ilić, Mirka
AU  - Ivanović-Matić, Svetlana
PY  - 2012
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6069
AB  - Aims: Diabetes-related oxidative stress conditions lead to progressive tissue damage and
disfunctionality. Mechanisms underlying liver pathophysiology during diabetes are not
fully understood. The aim of this study was to find relationship between diabetes-related
DNA damage in the rat liver and activities of prosurvival signaling pathways. Methods:
Diabetes, induced by single intraperitoneal injection of streptozotocin, was analyzed two
(development stage) and eight weeks after treatment (stable diabetes). Extent of DNA
damage, analysed by commet assay, was corelated with oxidative status (plasma level of
ROS, liver antioxidant capacity) and activity/abundance of kinases (Akt, p38, ERK1,
JNK, JAK) and transcription factors NF-kB p65 and STAT3. Results: Significant DNA
damage in development stage is accompanied by elevated plasma levels of O2
- and H2O2,
decreased activities of CAT, MnSOD, and GST in the liver and increased activation of
proapoptotic JNK signal pathway. Lower DNA damage in stable diabetes, is
accompanied by elevated plasma level of O2
-, restored antioxidative liver enzyme
activity, decreased activation of JNK and increased activation of prosurvival Akt and
ERK signal pathways. Conclusion: These findings indicate that level of DNA damage in
diabetic liver depends on the extent of oxidative stress, antioxidant activity and balance
between JNK and Akt/ERK signal pathways activation.
PB  - Karger Publishers
T2  - Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
T1  - Activation Level of JNK and Akt/ERK Signaling Pathways Determinates Extent of DNA Damage in the Liver of Diabetic Rats
IS  - 3
VL  - 30
DO  - 10.1159/000341452
SP  - 723
EP  - 734
ER  - 

@article{
author = "Martinović, Vesna and Grigorov, Ilijana and Bogojević, Desanka and Petrović, Anja and Jovanović Stojanov, Sofija and Ilić, Mirka and Ivanović-Matić, Svetlana",
year = "2012",
abstract = "Aims: Diabetes-related oxidative stress conditions lead to progressive tissue damage and
disfunctionality. Mechanisms underlying liver pathophysiology during diabetes are not
fully understood. The aim of this study was to find relationship between diabetes-related
DNA damage in the rat liver and activities of prosurvival signaling pathways. Methods:
Diabetes, induced by single intraperitoneal injection of streptozotocin, was analyzed two
(development stage) and eight weeks after treatment (stable diabetes). Extent of DNA
damage, analysed by commet assay, was corelated with oxidative status (plasma level of
ROS, liver antioxidant capacity) and activity/abundance of kinases (Akt, p38, ERK1,
JNK, JAK) and transcription factors NF-kB p65 and STAT3. Results: Significant DNA
damage in development stage is accompanied by elevated plasma levels of O2
- and H2O2,
decreased activities of CAT, MnSOD, and GST in the liver and increased activation of
proapoptotic JNK signal pathway. Lower DNA damage in stable diabetes, is
accompanied by elevated plasma level of O2
-, restored antioxidative liver enzyme
activity, decreased activation of JNK and increased activation of prosurvival Akt and
ERK signal pathways. Conclusion: These findings indicate that level of DNA damage in
diabetic liver depends on the extent of oxidative stress, antioxidant activity and balance
between JNK and Akt/ERK signal pathways activation.",
publisher = "Karger Publishers",
journal = "Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology",
title = "Activation Level of JNK and Akt/ERK Signaling Pathways Determinates Extent of DNA Damage in the Liver of Diabetic Rats",
number = "3",
volume = "30",
doi = "10.1159/000341452",
pages = "723-734"
}

Martinović, V., Grigorov, I., Bogojević, D., Petrović, A., Jovanović Stojanov, S., Ilić, M.,& Ivanović-Matić, S.. (2012). Activation Level of JNK and Akt/ERK Signaling Pathways Determinates Extent of DNA Damage in the Liver of Diabetic Rats. in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
Karger Publishers., 30(3), 723-734.
https://doi.org/10.1159/000341452

Martinović V, Grigorov I, Bogojević D, Petrović A, Jovanović Stojanov S, Ilić M, Ivanović-Matić S. Activation Level of JNK and Akt/ERK Signaling Pathways Determinates Extent of DNA Damage in the Liver of Diabetic Rats. in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology. 2012;30(3):723-734.
doi:10.1159/000341452 .

Martinović, Vesna, Grigorov, Ilijana, Bogojević, Desanka, Petrović, Anja, Jovanović Stojanov, Sofija, Ilić, Mirka, Ivanović-Matić, Svetlana, "Activation Level of JNK and Akt/ERK Signaling Pathways Determinates Extent of DNA Damage in the Liver of Diabetic Rats" in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 30, no. 3 (2012):723-734,
https://doi.org/10.1159/000341452 . .