TY  - JOUR
AU  - Đurašević, Siniša
AU  - Stojković, Maja
AU  - Sopta, Jelena
AU  - Pavlović, Slađan
AU  - Borković Mitić, Slavica
AU  - Ivanović, Anđelija
AU  - Jasnić, Nebojša
AU  - Tosti, Tomislav
AU  - Đurović, Saša
AU  - Đorđević, Jelena
AU  - Todorović, Zoran
PY  - 2021
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4090
AB  - Acute ischemia/reperfusion (I/R) liver injury is a clinical condition challenging to treat. Meldonium
is an anti‑ischemic agent that shifts energy production from fatty acid oxidation to less oxygen‑
consuming glycolysis. Thus, we investigated the effects of a 4‑week meldonium pre‑treatment
(300 mg/kg b.m./day) on the acute I/R liver injury in Wistar strain male rats. Our results showed that
meldonium ameliorates I/R‑induced liver inflammation and injury, as confirmed by liver histology,
and by attenuation of serum alanine‑ and aspartate aminotransferase activity, serum and liver
high mobility group box 1 protein expression, and liver expression of Bax/Bcl2, haptoglobin, and
the phosphorylated nuclear factor kappa‑light‑chain‑enhancer of activated B cells. Through the
increased hepatic activation of the nuclear factor erythroid 2‑related factor 2, meldonium improves
the antioxidative defence in the liver of animals subjected to I/R, as proved by an increase in serum
and liver ascorbic/dehydroascorbic acid ratio, hepatic haem oxygenase 1 expression, glutathione
and free thiol groups content, and hepatic copper‑zinc superoxide dismutase, manganese superoxide
dismutase, catalase, glutathione peroxidase, and glutathione reductase activity. Based on our results,
it can be concluded that meldonium represent a protective agent against I/R‑induced liver injury, with
a clinical significance in surgical procedures.
PB  - Nature Publishing Group
T2  - Scientific Reports
T1  - The effects of meldonium on the acute ischemia/reperfusion liver injury in rats
IS  - 1
VL  - 11
DO  - 10.1038/s41598-020-80011-y
SP  - 1305
ER  - 

@article{
author = "Đurašević, Siniša and Stojković, Maja and Sopta, Jelena and Pavlović, Slađan and Borković Mitić, Slavica and Ivanović, Anđelija and Jasnić, Nebojša and Tosti, Tomislav and Đurović, Saša and Đorđević, Jelena and Todorović, Zoran",
year = "2021",
abstract = "Acute ischemia/reperfusion (I/R) liver injury is a clinical condition challenging to treat. Meldonium
is an anti‑ischemic agent that shifts energy production from fatty acid oxidation to less oxygen‑
consuming glycolysis. Thus, we investigated the effects of a 4‑week meldonium pre‑treatment
(300 mg/kg b.m./day) on the acute I/R liver injury in Wistar strain male rats. Our results showed that
meldonium ameliorates I/R‑induced liver inflammation and injury, as confirmed by liver histology,
and by attenuation of serum alanine‑ and aspartate aminotransferase activity, serum and liver
high mobility group box 1 protein expression, and liver expression of Bax/Bcl2, haptoglobin, and
the phosphorylated nuclear factor kappa‑light‑chain‑enhancer of activated B cells. Through the
increased hepatic activation of the nuclear factor erythroid 2‑related factor 2, meldonium improves
the antioxidative defence in the liver of animals subjected to I/R, as proved by an increase in serum
and liver ascorbic/dehydroascorbic acid ratio, hepatic haem oxygenase 1 expression, glutathione
and free thiol groups content, and hepatic copper‑zinc superoxide dismutase, manganese superoxide
dismutase, catalase, glutathione peroxidase, and glutathione reductase activity. Based on our results,
it can be concluded that meldonium represent a protective agent against I/R‑induced liver injury, with
a clinical significance in surgical procedures.",
publisher = "Nature Publishing Group",
journal = "Scientific Reports",
title = "The effects of meldonium on the acute ischemia/reperfusion liver injury in rats",
number = "1",
volume = "11",
doi = "10.1038/s41598-020-80011-y",
pages = "1305"
}

Đurašević, S., Stojković, M., Sopta, J., Pavlović, S., Borković Mitić, S., Ivanović, A., Jasnić, N., Tosti, T., Đurović, S., Đorđević, J.,& Todorović, Z.. (2021). The effects of meldonium on the acute ischemia/reperfusion liver injury in rats. in Scientific Reports
Nature Publishing Group., 11(1), 1305.
https://doi.org/10.1038/s41598-020-80011-y

Đurašević S, Stojković M, Sopta J, Pavlović S, Borković Mitić S, Ivanović A, Jasnić N, Tosti T, Đurović S, Đorđević J, Todorović Z. The effects of meldonium on the acute ischemia/reperfusion liver injury in rats. in Scientific Reports. 2021;11(1):1305.
doi:10.1038/s41598-020-80011-y .

Đurašević, Siniša, Stojković, Maja, Sopta, Jelena, Pavlović, Slađan, Borković Mitić, Slavica, Ivanović, Anđelija, Jasnić, Nebojša, Tosti, Tomislav, Đurović, Saša, Đorđević, Jelena, Todorović, Zoran, "The effects of meldonium on the acute ischemia/reperfusion liver injury in rats" in Scientific Reports, 11, no. 1 (2021):1305,
https://doi.org/10.1038/s41598-020-80011-y . .

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 . .