TY  - JOUR
AU  - Momčilović, Miljana
AU  - Miljković, Đorđe
AU  - Mostarica-Stojković, Marija B
PY  - 2009
PY  - 2009
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/216
AB  - Brain endothelial cells (BEC) are the major constituents of the blood-brain barrier (BBB), the structure that controls entrance of immune cells into CNS parenchyma. Our aim was to investigate the influence of BEC on production of IL-17 and IFN-γ-cytokines that are important for CNS inflammation. To that end, co-cultivations of the bEnd.3 brain endothelial cell line and lymph node cells (LNC) were performed, and gene expression and production of IL-17 and IFN-γ were determined. It was found that bEnd.3 cells inhibited expression and production of IFN-γ, but not of IL-17. Additionally, bEnd.3 cells also reduced production of the major IFN-γ-promoting cytokine - IL-12 - in LNC. The observed variation in modulation of pro-inflammatory cytokines by BEC could be of importance for the understanding of CNS inflammation.
AB  - Ćelije moždanog endotela su osnovni elementi građe krvno moždane barijere, strukture koja kontroliše ulazak ćelija imunskog sistema u parenhim CNS. Naš cilj je bio da se ispita uticaj ovih ćelija na produkciju interferona-gama i interleukina 17, kao ključnih proinflamatornih citokina u neuroinflamaciji. Zbog toga smo vršili ko-kultivaciju bEnd.3 linije moždanog endotela i ćelija limfnog čvora, i to u prisustvu ili odsustvu direktnog kontakta među navedenim populacijama, i određivali ekspresiju gena i produkciju navedenih citokina. Pokazalo se da bEnd.3 ćelije potentno inhibiraju produkciju interferona-gama, ali ne i interleukina-17. Takođe, merili smo i produkciju interleukina-12, glavnog stimulatornog citokina za produkciju interferona-gama, i pokazali da je i njegova produkcija smanjena u ko-kultivaciji bEnd.3 ćelija i ćelija limfnog čvora. Zapažena različitost u delovanju ćelija moždanog Endotela na dva osnovna proinflamatorna citokina je od Značaja za razumevanje kompleksnog procesa regulacije inflamacije u CNS.
T2  - Archives of Biological Sciences
T1  - Ćelije mišjeg moždanog endotela ostvaruju različit uticaj na produkciju interferona-γ i interleukina-17 in vitro
T1  - Murine brain endothelial cells differently modulate interferon-γ and interleukin-17 production in vitro
IS  - 1
VL  - 61
DO  - 10.2298/ABS0901029M
SP  - 29
EP  - 36
ER  - 

@article{
author = "Momčilović, Miljana and Miljković, Đorđe and Mostarica-Stojković, Marija B",
year = "2009, 2009",
abstract = "Brain endothelial cells (BEC) are the major constituents of the blood-brain barrier (BBB), the structure that controls entrance of immune cells into CNS parenchyma. Our aim was to investigate the influence of BEC on production of IL-17 and IFN-γ-cytokines that are important for CNS inflammation. To that end, co-cultivations of the bEnd.3 brain endothelial cell line and lymph node cells (LNC) were performed, and gene expression and production of IL-17 and IFN-γ were determined. It was found that bEnd.3 cells inhibited expression and production of IFN-γ, but not of IL-17. Additionally, bEnd.3 cells also reduced production of the major IFN-γ-promoting cytokine - IL-12 - in LNC. The observed variation in modulation of pro-inflammatory cytokines by BEC could be of importance for the understanding of CNS inflammation., Ćelije moždanog endotela su osnovni elementi građe krvno moždane barijere, strukture koja kontroliše ulazak ćelija imunskog sistema u parenhim CNS. Naš cilj je bio da se ispita uticaj ovih ćelija na produkciju interferona-gama i interleukina 17, kao ključnih proinflamatornih citokina u neuroinflamaciji. Zbog toga smo vršili ko-kultivaciju bEnd.3 linije moždanog endotela i ćelija limfnog čvora, i to u prisustvu ili odsustvu direktnog kontakta među navedenim populacijama, i određivali ekspresiju gena i produkciju navedenih citokina. Pokazalo se da bEnd.3 ćelije potentno inhibiraju produkciju interferona-gama, ali ne i interleukina-17. Takođe, merili smo i produkciju interleukina-12, glavnog stimulatornog citokina za produkciju interferona-gama, i pokazali da je i njegova produkcija smanjena u ko-kultivaciji bEnd.3 ćelija i ćelija limfnog čvora. Zapažena različitost u delovanju ćelija moždanog Endotela na dva osnovna proinflamatorna citokina je od Značaja za razumevanje kompleksnog procesa regulacije inflamacije u CNS.",
journal = "Archives of Biological Sciences",
title = "Ćelije mišjeg moždanog endotela ostvaruju različit uticaj na produkciju interferona-γ i interleukina-17 in vitro, Murine brain endothelial cells differently modulate interferon-γ and interleukin-17 production in vitro",
number = "1",
volume = "61",
doi = "10.2298/ABS0901029M",
pages = "29-36"
}

Momčilović, M., Miljković, Đ.,& Mostarica-Stojković, M. B.. (2009). Ćelije mišjeg moždanog endotela ostvaruju različit uticaj na produkciju interferona-γ i interleukina-17 in vitro. in Archives of Biological Sciences, 61(1), 29-36.
https://doi.org/10.2298/ABS0901029M

Momčilović M, Miljković Đ, Mostarica-Stojković MB. Ćelije mišjeg moždanog endotela ostvaruju različit uticaj na produkciju interferona-γ i interleukina-17 in vitro. in Archives of Biological Sciences. 2009;61(1):29-36.
doi:10.2298/ABS0901029M .

Momčilović, Miljana, Miljković, Đorđe, Mostarica-Stojković, Marija B, "Ćelije mišjeg moždanog endotela ostvaruju različit uticaj na produkciju interferona-γ i interleukina-17 in vitro" in Archives of Biological Sciences, 61, no. 1 (2009):29-36,
https://doi.org/10.2298/ABS0901029M . .

TY  - JOUR
AU  - Lavrnja, Irena
AU  - Savić, Danijela
AU  - Bjelobaba, Ivana
AU  - Peković, Sanja
AU  - Dacić, Sanja
AU  - Nedeljković, Nadežda N.
AU  - Mostarica-Stojković, Marija B.
AU  - Stošić-Grujičić, Stanislava
AU  - Rakić, Ljubisav
AU  - Stojiljković, Mirjana B.
PY  - 2008
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1141
AB  - To determine the mechanism underlying ribavirin induced amelioration of experimental autoimmune encephalomyelitis (EAE), cytokine profiles were evaluated in draining lymph node (DLN) cell culture supernatants and spinal cord obtained from EAE and/or ribavirin-treated EAE Dark Agouti rats. Administration of ribavirin to EAE rats markedly affected the production of pro-inflammatory cytokines IFN-gamma, IL-1 beta and TNF-alpha in DLN and spinal cord, thus shifting the balance towards the anti-inflammatory cytokines IL-10 and TGF-beta. These findings suggest that ribavirin attenuates EAE by limiting cytokine-mediated immunoinflammatory events leading to CNS destruction. The conducted experiments provide rationale for ribavirin to be considered as a candidate drug in the development of new therapeutic strategies for the treatment of autoimmune diseases in humans, such as multiple sclerosis. (c) 2008 Elsevier B.V. All rights reserved.
PB  - Amsterdam, Netherlands: Elsevier
T2  - International Immunopharmacology
T1  - Ribavirin ameliorates experimental autoimmune encephalomyelitis in rats and modulates cytokine production
IS  - 9
VL  - 8
DO  - 10.1016/j.intimp.2008.05.008
SP  - 1282
EP  - 1290
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1141
ER  - 

@article{
author = "Lavrnja, Irena and Savić, Danijela and Bjelobaba, Ivana and Peković, Sanja and Dacić, Sanja and Nedeljković, Nadežda N. and Mostarica-Stojković, Marija B. and Stošić-Grujičić, Stanislava and Rakić, Ljubisav and Stojiljković, Mirjana B.",
year = "2008",
abstract = "To determine the mechanism underlying ribavirin induced amelioration of experimental autoimmune encephalomyelitis (EAE), cytokine profiles were evaluated in draining lymph node (DLN) cell culture supernatants and spinal cord obtained from EAE and/or ribavirin-treated EAE Dark Agouti rats. Administration of ribavirin to EAE rats markedly affected the production of pro-inflammatory cytokines IFN-gamma, IL-1 beta and TNF-alpha in DLN and spinal cord, thus shifting the balance towards the anti-inflammatory cytokines IL-10 and TGF-beta. These findings suggest that ribavirin attenuates EAE by limiting cytokine-mediated immunoinflammatory events leading to CNS destruction. The conducted experiments provide rationale for ribavirin to be considered as a candidate drug in the development of new therapeutic strategies for the treatment of autoimmune diseases in humans, such as multiple sclerosis. (c) 2008 Elsevier B.V. All rights reserved.",
publisher = "Amsterdam, Netherlands: Elsevier",
journal = "International Immunopharmacology",
title = "Ribavirin ameliorates experimental autoimmune encephalomyelitis in rats and modulates cytokine production",
number = "9",
volume = "8",
doi = "10.1016/j.intimp.2008.05.008",
pages = "1282-1290",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1141"
}

Lavrnja, I., Savić, D., Bjelobaba, I., Peković, S., Dacić, S., Nedeljković, N. N., Mostarica-Stojković, M. B., Stošić-Grujičić, S., Rakić, L.,& Stojiljković, M. B.. (2008). Ribavirin ameliorates experimental autoimmune encephalomyelitis in rats and modulates cytokine production. in International Immunopharmacology
Amsterdam, Netherlands: Elsevier., 8(9), 1282-1290.
https://doi.org/10.1016/j.intimp.2008.05.008
https://hdl.handle.net/21.15107/rcub_ibiss_1141

Lavrnja I, Savić D, Bjelobaba I, Peković S, Dacić S, Nedeljković NN, Mostarica-Stojković MB, Stošić-Grujičić S, Rakić L, Stojiljković MB. Ribavirin ameliorates experimental autoimmune encephalomyelitis in rats and modulates cytokine production. in International Immunopharmacology. 2008;8(9):1282-1290.
doi:10.1016/j.intimp.2008.05.008
https://hdl.handle.net/21.15107/rcub_ibiss_1141 .

Lavrnja, Irena, Savić, Danijela, Bjelobaba, Ivana, Peković, Sanja, Dacić, Sanja, Nedeljković, Nadežda N., Mostarica-Stojković, Marija B., Stošić-Grujičić, Stanislava, Rakić, Ljubisav, Stojiljković, Mirjana B., "Ribavirin ameliorates experimental autoimmune encephalomyelitis in rats and modulates cytokine production" in International Immunopharmacology, 8, no. 9 (2008):1282-1290,
https://doi.org/10.1016/j.intimp.2008.05.008 .,
https://hdl.handle.net/21.15107/rcub_ibiss_1141 .

TY  - JOUR
AU  - Harhaji-Trajković, Ljubica
AU  - Isaković, Aleksandra
AU  - Zogović, Nevena
AU  - Marković, Zoran
AU  - Todorović-Marković, Biljana
AU  - Nikolić, Nadežda
AU  - Vranješ-Đurić, Sanja
AU  - Marković, Ivanka
AU  - Trajković, Vladimir
PY  - 2007
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6544
AB  - Using the rat glioma cell line C6 and the human glioma cell line U251, we demonstrate the multiple mechanisms underlying the in vitro anticancer effects of the C(60) fullerene water suspension (nano-C(60) or nC(60)) produced by solvent exchange method. Nano-C(60) in a dose-dependent manner reduced the tumor cell numbers after 24 h of incubation. The observed antiglioma action of nC(60) at high concentration (1 microg/ml) was due to a reactive oxygen species-mediated necrotic cell damage that was partly dependent on oxidative stress-induced activation of extracellular signal-regulated kinase (ERK). On the other hand, low-dose nC(60) (0.25 microg/ml) did not induce either necrotic or apoptotic cell death, but caused oxidative stress/ERK-independent cell cycle block in G(2)/M phase and subsequent inhibition of tumor cell proliferation. Treatment with either high-dose or low-dose nC(60) caused the appearance of acidified intracytoplasmic vesicles indicative of autophagy, but only the antiglioma effect of low-dose nC(60) was significantly attenuated by inhibiting autophagy with bafilomycin A1. Importantly, primary rat astrocytes were less sensitive than their transformed counterparts to a cytostatic action of low-dose nC(60). These data provide grounds for further development of nC(60) as an anticancer agent.
PB  - Elsevier BV
T2  - European Journal of Pharmacology
T1  - Multiple mechanisms underlying the anticancer action of nanocrystalline fullerene
IS  - 1-3
VL  - 568
DO  - 10.1016/j.ejphar.2007.04.041
SP  - 89
EP  - 98
ER  - 

@article{
author = "Harhaji-Trajković, Ljubica and Isaković, Aleksandra and Zogović, Nevena and Marković, Zoran and Todorović-Marković, Biljana and Nikolić, Nadežda and Vranješ-Đurić, Sanja and Marković, Ivanka and Trajković, Vladimir",
year = "2007",
abstract = "Using the rat glioma cell line C6 and the human glioma cell line U251, we demonstrate the multiple mechanisms underlying the in vitro anticancer effects of the C(60) fullerene water suspension (nano-C(60) or nC(60)) produced by solvent exchange method. Nano-C(60) in a dose-dependent manner reduced the tumor cell numbers after 24 h of incubation. The observed antiglioma action of nC(60) at high concentration (1 microg/ml) was due to a reactive oxygen species-mediated necrotic cell damage that was partly dependent on oxidative stress-induced activation of extracellular signal-regulated kinase (ERK). On the other hand, low-dose nC(60) (0.25 microg/ml) did not induce either necrotic or apoptotic cell death, but caused oxidative stress/ERK-independent cell cycle block in G(2)/M phase and subsequent inhibition of tumor cell proliferation. Treatment with either high-dose or low-dose nC(60) caused the appearance of acidified intracytoplasmic vesicles indicative of autophagy, but only the antiglioma effect of low-dose nC(60) was significantly attenuated by inhibiting autophagy with bafilomycin A1. Importantly, primary rat astrocytes were less sensitive than their transformed counterparts to a cytostatic action of low-dose nC(60). These data provide grounds for further development of nC(60) as an anticancer agent.",
publisher = "Elsevier BV",
journal = "European Journal of Pharmacology",
title = "Multiple mechanisms underlying the anticancer action of nanocrystalline fullerene",
number = "1-3",
volume = "568",
doi = "10.1016/j.ejphar.2007.04.041",
pages = "89-98"
}

Harhaji-Trajković, L., Isaković, A., Zogović, N., Marković, Z., Todorović-Marković, B., Nikolić, N., Vranješ-Đurić, S., Marković, I.,& Trajković, V.. (2007). Multiple mechanisms underlying the anticancer action of nanocrystalline fullerene. in European Journal of Pharmacology
Elsevier BV., 568(1-3), 89-98.
https://doi.org/10.1016/j.ejphar.2007.04.041

Harhaji-Trajković L, Isaković A, Zogović N, Marković Z, Todorović-Marković B, Nikolić N, Vranješ-Đurić S, Marković I, Trajković V. Multiple mechanisms underlying the anticancer action of nanocrystalline fullerene. in European Journal of Pharmacology. 2007;568(1-3):89-98.
doi:10.1016/j.ejphar.2007.04.041 .

Harhaji-Trajković, Ljubica, Isaković, Aleksandra, Zogović, Nevena, Marković, Zoran, Todorović-Marković, Biljana, Nikolić, Nadežda, Vranješ-Đurić, Sanja, Marković, Ivanka, Trajković, Vladimir, "Multiple mechanisms underlying the anticancer action of nanocrystalline fullerene" in European Journal of Pharmacology, 568, no. 1-3 (2007):89-98,
https://doi.org/10.1016/j.ejphar.2007.04.041 . .

TY  - JOUR
AU  - Stošić-Grujičić, Stanislava
AU  - Stojanović, Ivana D.
AU  - Mangano,  Katia
AU  - Fresta, Massimo
AU  - Maksimović-Ivanić, Danijela
AU  - Harhaji-Trajković, Ljubica
AU  - Popadić, Dušan
AU  - Momčilović, Miljana
AU  - Miljković, Đorđe
AU  - Kim, Joseph
AU  - Al-Abed, Yousef
AU  - Nicoletti,  Ferdinando
PY  - 2007
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3824
AB  - (S,R)-3-Phenyl-4,5-dihydro-5-isoxasole acetic acid (VGX-1027) is an isoxazole compound that exhibits various immunomodulatory properties. The capacity of VGX-1027 to prevent interleukin (IL)-1beta plus interferon-gamma-induced pancreatic islet death in vitro prompted us to evaluate its effects on the development of autoimmune diabetes in preclinical models of human type 1 diabetes mellitus (T1D). Administration of VGX-1027 to NOD mice with spontaneous or accelerated forms of diabetes induced either by injection of cyclophosphamide or by transfer of spleen cells from acutely diabetic syngeneic donors markedly reduced the cumulative incidence of diabetes and insulitis. In addition, VGX-1027 given either i.p. or p.o. to CBA/H mice made diabetic with multiple low doses of streptozotocin successfully counteracted the development of destructive insulitis and hyperglycemia. The animals receiving VGX-1027 exhibited reduced production of the proinflammatory mediators tumor necrosis factor-alpha, IL-1beta, macrophage migration inhibitory factor, and inducible nitric-oxide synthase-mediated nitric oxide generation in both pancreatic islets and peripheral compartments. These results indicate that VGX-1027 probably exerts its antidiabetogenic effects by limiting cytokine-mediated immunoinflammatory events, leading to inflammation and destruction of pancreatic islets. VGX-1027 seems worthy of being considered as a candidate drug in the development of new therapeutic strategies for the prevention and early treatment of T1D.
PB  - Rockville: American Society for Pharmacology and Experimental Therapeutics (ASPET)
T2  - Journal of Pharmacology and Experimental Therapeutics
T1  - A potent immunomodulatory compound, (S,R)-3-Phenyl-4,5-dihydro-5-isoxazole acetic acid, prevents spontaneous and accelerated forms of autoimmune diabetes in NOD mice and inhibits the immunoinflammatory diabetes induced by multiple low doses of streptozotocin in CBA/H mice
IS  - 3
VL  - 320
DO  - 10.1124/jpet.106.109272
SP  - 1038
EP  - 1049
ER  - 

@article{
author = "Stošić-Grujičić, Stanislava and Stojanović, Ivana D. and Mangano,  Katia and Fresta, Massimo and Maksimović-Ivanić, Danijela and Harhaji-Trajković, Ljubica and Popadić, Dušan and Momčilović, Miljana and Miljković, Đorđe and Kim, Joseph and Al-Abed, Yousef and Nicoletti,  Ferdinando",
year = "2007",
abstract = "(S,R)-3-Phenyl-4,5-dihydro-5-isoxasole acetic acid (VGX-1027) is an isoxazole compound that exhibits various immunomodulatory properties. The capacity of VGX-1027 to prevent interleukin (IL)-1beta plus interferon-gamma-induced pancreatic islet death in vitro prompted us to evaluate its effects on the development of autoimmune diabetes in preclinical models of human type 1 diabetes mellitus (T1D). Administration of VGX-1027 to NOD mice with spontaneous or accelerated forms of diabetes induced either by injection of cyclophosphamide or by transfer of spleen cells from acutely diabetic syngeneic donors markedly reduced the cumulative incidence of diabetes and insulitis. In addition, VGX-1027 given either i.p. or p.o. to CBA/H mice made diabetic with multiple low doses of streptozotocin successfully counteracted the development of destructive insulitis and hyperglycemia. The animals receiving VGX-1027 exhibited reduced production of the proinflammatory mediators tumor necrosis factor-alpha, IL-1beta, macrophage migration inhibitory factor, and inducible nitric-oxide synthase-mediated nitric oxide generation in both pancreatic islets and peripheral compartments. These results indicate that VGX-1027 probably exerts its antidiabetogenic effects by limiting cytokine-mediated immunoinflammatory events, leading to inflammation and destruction of pancreatic islets. VGX-1027 seems worthy of being considered as a candidate drug in the development of new therapeutic strategies for the prevention and early treatment of T1D.",
publisher = "Rockville: American Society for Pharmacology and Experimental Therapeutics (ASPET)",
journal = "Journal of Pharmacology and Experimental Therapeutics",
title = "A potent immunomodulatory compound, (S,R)-3-Phenyl-4,5-dihydro-5-isoxazole acetic acid, prevents spontaneous and accelerated forms of autoimmune diabetes in NOD mice and inhibits the immunoinflammatory diabetes induced by multiple low doses of streptozotocin in CBA/H mice",
number = "3",
volume = "320",
doi = "10.1124/jpet.106.109272",
pages = "1038-1049"
}

Stošić-Grujičić, S., Stojanović, I. D., Mangano,  ., Fresta, M., Maksimović-Ivanić, D., Harhaji-Trajković, L., Popadić, D., Momčilović, M., Miljković, Đ., Kim, J., Al-Abed, Y.,& Nicoletti,  .. (2007). A potent immunomodulatory compound, (S,R)-3-Phenyl-4,5-dihydro-5-isoxazole acetic acid, prevents spontaneous and accelerated forms of autoimmune diabetes in NOD mice and inhibits the immunoinflammatory diabetes induced by multiple low doses of streptozotocin in CBA/H mice. in Journal of Pharmacology and Experimental Therapeutics
Rockville: American Society for Pharmacology and Experimental Therapeutics (ASPET)., 320(3), 1038-1049.
https://doi.org/10.1124/jpet.106.109272

Stošić-Grujičić S, Stojanović ID, Mangano  , Fresta M, Maksimović-Ivanić D, Harhaji-Trajković L, Popadić D, Momčilović M, Miljković Đ, Kim J, Al-Abed Y, Nicoletti  . A potent immunomodulatory compound, (S,R)-3-Phenyl-4,5-dihydro-5-isoxazole acetic acid, prevents spontaneous and accelerated forms of autoimmune diabetes in NOD mice and inhibits the immunoinflammatory diabetes induced by multiple low doses of streptozotocin in CBA/H mice. in Journal of Pharmacology and Experimental Therapeutics. 2007;320(3):1038-1049.
doi:10.1124/jpet.106.109272 .

Stošić-Grujičić, Stanislava, Stojanović, Ivana D., Mangano,  Katia, Fresta, Massimo, Maksimović-Ivanić, Danijela, Harhaji-Trajković, Ljubica, Popadić, Dušan, Momčilović, Miljana, Miljković, Đorđe, Kim, Joseph, Al-Abed, Yousef, Nicoletti,  Ferdinando, "A potent immunomodulatory compound, (S,R)-3-Phenyl-4,5-dihydro-5-isoxazole acetic acid, prevents spontaneous and accelerated forms of autoimmune diabetes in NOD mice and inhibits the immunoinflammatory diabetes induced by multiple low doses of streptozotocin in CBA/H mice" in Journal of Pharmacology and Experimental Therapeutics, 320, no. 3 (2007):1038-1049,
https://doi.org/10.1124/jpet.106.109272 . .

TY  - JOUR
AU  - Harhaji-Trajković, Ljubica
AU  - Mijatović, Sanja
AU  - Maksimović-Ivanić, Danijela
AU  - Popadić, Dusan
AU  - Isaković,  Aleksandra
AU  - Todorović-Marković, Biljana
AU  - Trajković, Vladimir
PY  - 2007
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3825
AB  - We demonstrate the capacity of an herbal anthraquinone aloe emodin to reduce the cytotoxicity of the proinflammatory cytokine tumor necrosis factor (TNF) towards L929 mouse fibrosarcoma and U251 human glioma cell lines. Aloe emodin inhibited both TNF-induced cell necrosis and apoptosis, but it did not reduce cell death induced by UV radiation or hydrogen peroxide. Aloe emodin inhibited both basal and TNF-triggered activation of extracellular signal-regulated kinase (ERK), and a selective blockade of ERK activation mimicked the cytoprotective action of the drug. On the other hand, aloe emodin did not affect TNF-induced activation of p38 mitogen-activated protein kinase or generation of reactive oxygen species. The combination of aloe emodin and TNF caused an intracellular appearance of acidified autophagic vesicles, and the inhibition of autophagy with bafilomycin or 3-methyladenine efficiently blocked the cytoprotective action of aloe emodin. These data indicate that aloe emodin could prevent TNF-triggered cell death through mechanisms involving induction of autophagy and blockade of ERK activation.
PB  - Amsterdam: Elsevier
T2  - European Journal of Pharmacology
T1  - Aloe emodin inhibits the cytotoxic action of tumor necrosis factor
IS  - 1-3
VL  - 568
VL  - 568
DO  - 10.1016/j.ejphar.2007.04.029
SP  - 248
EP  - 259
ER  - 

@article{
author = "Harhaji-Trajković, Ljubica and Mijatović, Sanja and Maksimović-Ivanić, Danijela and Popadić, Dusan and Isaković,  Aleksandra and Todorović-Marković, Biljana and Trajković, Vladimir",
year = "2007",
abstract = "We demonstrate the capacity of an herbal anthraquinone aloe emodin to reduce the cytotoxicity of the proinflammatory cytokine tumor necrosis factor (TNF) towards L929 mouse fibrosarcoma and U251 human glioma cell lines. Aloe emodin inhibited both TNF-induced cell necrosis and apoptosis, but it did not reduce cell death induced by UV radiation or hydrogen peroxide. Aloe emodin inhibited both basal and TNF-triggered activation of extracellular signal-regulated kinase (ERK), and a selective blockade of ERK activation mimicked the cytoprotective action of the drug. On the other hand, aloe emodin did not affect TNF-induced activation of p38 mitogen-activated protein kinase or generation of reactive oxygen species. The combination of aloe emodin and TNF caused an intracellular appearance of acidified autophagic vesicles, and the inhibition of autophagy with bafilomycin or 3-methyladenine efficiently blocked the cytoprotective action of aloe emodin. These data indicate that aloe emodin could prevent TNF-triggered cell death through mechanisms involving induction of autophagy and blockade of ERK activation.",
publisher = "Amsterdam: Elsevier",
journal = "European Journal of Pharmacology",
title = "Aloe emodin inhibits the cytotoxic action of tumor necrosis factor",
number = "1-3",
volume = "568, 568",
doi = "10.1016/j.ejphar.2007.04.029",
pages = "248-259"
}

Harhaji-Trajković, L., Mijatović, S., Maksimović-Ivanić, D., Popadić, D., Isaković,  ., Todorović-Marković, B.,& Trajković, V.. (2007). Aloe emodin inhibits the cytotoxic action of tumor necrosis factor. in European Journal of Pharmacology
Amsterdam: Elsevier., 568(1-3), 248-259.
https://doi.org/10.1016/j.ejphar.2007.04.029

Harhaji-Trajković L, Mijatović S, Maksimović-Ivanić D, Popadić D, Isaković  , Todorović-Marković B, Trajković V. Aloe emodin inhibits the cytotoxic action of tumor necrosis factor. in European Journal of Pharmacology. 2007;568(1-3):248-259.
doi:10.1016/j.ejphar.2007.04.029 .

Harhaji-Trajković, Ljubica, Mijatović, Sanja, Maksimović-Ivanić, Danijela, Popadić, Dusan, Isaković,  Aleksandra, Todorović-Marković, Biljana, Trajković, Vladimir, "Aloe emodin inhibits the cytotoxic action of tumor necrosis factor" in European Journal of Pharmacology, 568, no. 1-3 (2007):248-259,
https://doi.org/10.1016/j.ejphar.2007.04.029 . .

TY  - CONF
AU  - Savić, Danijela
AU  - Lavrnja, Irena
AU  - Peković, Sanja
AU  - Šubašić, Sanja A
AU  - Jovanović, Sasa
AU  - Nikić, Ivana
AU  - Bjelobaba, Ivana
AU  - Mostarica-Stojković, Marija B
AU  - Stošić-Grujičić, Stanislava
AU  - Rakić, Ljubisav
AU  - Stojiljković, Mirjana B
PY  - 2006
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1636
AB  - Experimental autoimmune encephalomyelitis (EAE) is an animal model
of human disease multiple sclerosis (MS). Clinical signs of EAE are result of
an autoaggressive T-cell response against myelin. We have previously
shown that combined treatment with nucleoside analogues (ribavirin — R
+tiazofurin — T), inosine monophosphate dehydrogenase inhibitors,
ameliorates clinical signs and histological lesions of EAE in susceptible
rats, when they are given preventatively. The aim of this study was to
investigate the effect of combined treatment with R+T, given with the
appearance of first EAE clinical sign, on microglia and astrocytes response.
These cells of the target tissue also participate in an autoimmune process.
The disease was induced in Dark Agouti rats with rat spinal cord
homogenate and had acute monophasic course. Ribavirin and tiazofurin
were given at a dosage of 30 mg/kg/day and 10 mg/kg every other day, for
15 days, respectively. Control group was immunized and treated with saline.
Amelioration of clinical signs and faster recovery was shown in group
treated with combination of R and T in comparison to control group.
Immunohistochemical analysis of the spinal cord tissue isolated after
15 days of combined therapy revealed decrease in vimentin positive cells
and microglia compared to control group. Additionally, morphology of
GFAP positive (glial fibrillary acid protein) cells and microglia indicated to
reactive type of these cells in control group. Results of this study revealed that R and T modulate glial response and have EAE protective effects when
they are given from the onset of disease.
C3  - 8th ISNI Congress; 2006 Oct 15-19; Nagoya, Japan
T1  - Nucleoside analogues effect on glial response in experimental autoimmune encephalomyelitis
SP  - 167
EP  - 168
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1636
ER  - 

@conference{
author = "Savić, Danijela and Lavrnja, Irena and Peković, Sanja and Šubašić, Sanja A and Jovanović, Sasa and Nikić, Ivana and Bjelobaba, Ivana and Mostarica-Stojković, Marija B and Stošić-Grujičić, Stanislava and Rakić, Ljubisav and Stojiljković, Mirjana B",
year = "2006",
abstract = "Experimental autoimmune encephalomyelitis (EAE) is an animal model
of human disease multiple sclerosis (MS). Clinical signs of EAE are result of
an autoaggressive T-cell response against myelin. We have previously
shown that combined treatment with nucleoside analogues (ribavirin — R
+tiazofurin — T), inosine monophosphate dehydrogenase inhibitors,
ameliorates clinical signs and histological lesions of EAE in susceptible
rats, when they are given preventatively. The aim of this study was to
investigate the effect of combined treatment with R+T, given with the
appearance of first EAE clinical sign, on microglia and astrocytes response.
These cells of the target tissue also participate in an autoimmune process.
The disease was induced in Dark Agouti rats with rat spinal cord
homogenate and had acute monophasic course. Ribavirin and tiazofurin
were given at a dosage of 30 mg/kg/day and 10 mg/kg every other day, for
15 days, respectively. Control group was immunized and treated with saline.
Amelioration of clinical signs and faster recovery was shown in group
treated with combination of R and T in comparison to control group.
Immunohistochemical analysis of the spinal cord tissue isolated after
15 days of combined therapy revealed decrease in vimentin positive cells
and microglia compared to control group. Additionally, morphology of
GFAP positive (glial fibrillary acid protein) cells and microglia indicated to
reactive type of these cells in control group. Results of this study revealed that R and T modulate glial response and have EAE protective effects when
they are given from the onset of disease.",
journal = "8th ISNI Congress; 2006 Oct 15-19; Nagoya, Japan",
title = "Nucleoside analogues effect on glial response in experimental autoimmune encephalomyelitis",
pages = "167-168",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1636"
}

Savić, D., Lavrnja, I., Peković, S., Šubašić, S. A., Jovanović, S., Nikić, I., Bjelobaba, I., Mostarica-Stojković, M. B., Stošić-Grujičić, S., Rakić, L.,& Stojiljković, M. B.. (2006). Nucleoside analogues effect on glial response in experimental autoimmune encephalomyelitis. in 8th ISNI Congress; 2006 Oct 15-19; Nagoya, Japan, 167-168.
https://hdl.handle.net/21.15107/rcub_ibiss_1636

Savić D, Lavrnja I, Peković S, Šubašić SA, Jovanović S, Nikić I, Bjelobaba I, Mostarica-Stojković MB, Stošić-Grujičić S, Rakić L, Stojiljković MB. Nucleoside analogues effect on glial response in experimental autoimmune encephalomyelitis. in 8th ISNI Congress; 2006 Oct 15-19; Nagoya, Japan. 2006;:167-168.
https://hdl.handle.net/21.15107/rcub_ibiss_1636 .

Savić, Danijela, Lavrnja, Irena, Peković, Sanja, Šubašić, Sanja A, Jovanović, Sasa, Nikić, Ivana, Bjelobaba, Ivana, Mostarica-Stojković, Marija B, Stošić-Grujičić, Stanislava, Rakić, Ljubisav, Stojiljković, Mirjana B, "Nucleoside analogues effect on glial response in experimental autoimmune encephalomyelitis" in 8th ISNI Congress; 2006 Oct 15-19; Nagoya, Japan (2006):167-168,
https://hdl.handle.net/21.15107/rcub_ibiss_1636 .