Milosavljević, P

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  • Milosavljević, P (2)
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Author's Bibliography

Suppression of experimental autoimmune myocarditis by sodium fusidate (fusidin)

Milenković, Marina; Vučićević, Dragana; Milosavljević, P; Arsenović-Ranin, Nevena; Stojić-Vukanić, Zorica; Čolić, Miodrag

(Academic Press Ltd- Elsevier Science Ltd, London, 2005)

TY  - JOUR
AU  - Milenković, Marina
AU  - Vučićević, Dragana
AU  - Milosavljević, P
AU  - Arsenović-Ranin, Nevena
AU  - Stojić-Vukanić, Zorica
AU  - Čolić, Miodrag
PY  - 2005
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/595
AB  - Fusidic acid and its sodium salt sodium fusidate (fusidin) are widely used antibiotics that possess immunomodulating properties. It has been shown that fusidin ameliorates the course of several organ-specific immunoinflammatory diseases and thus we investigated the effect of fusidin on myosin-induced experimental autoimmune myocarditis (EAM) in rats, a well-established animal model for human giant cell myocarditis and postmyocarditis dilated cardiomyopathy (DCM). Fusidin at doses of 80 mg kg(-1) was administrated i.m. to male Dark Agouti (DA) rats, either from days 0 to 10 (early treatment group), or from days 10 to 20 (late treatment group) after induction of EAM. Efficacy of fusidin treatment was determined on day 21 of EAM development. It was observed that both early and late treatment with fusidin markedly ameliorated clinical, histological and immunohistochemical signs of the disease. The treated rats had significantly decreased incidence of EAM, heart weight and heart weight/body weight ratio (Hw/Bw) compared with untreated animals. In contrast to the severe myocardial damage and cellular infiltration in the EAM rats, there was only focal infiltration of inflammatory cells in the myocardium of the treated rats. In both treated groups the mean microscopic score was markedly lower compared with vehicle-treated animals. In addition, the number of CD4+, ED1+ and OX6+ cells was significantly lower in myocardium of fusidin-treated rats than that in untreated group. The present findings suggest that fusidin exhibited both early and late therapeutical effect in EAM.
PB  - Academic Press Ltd- Elsevier Science Ltd, London
T2  - Pharmacological Research
T1  - Suppression of experimental autoimmune myocarditis by sodium fusidate (fusidin)
VL  - 52
IS  - 6
SP  - 491
EP  - 496
DO  - 10.1016/j.phrs.2005.08.001
ER  - 
@article{
author = "Milenković, Marina and Vučićević, Dragana and Milosavljević, P and Arsenović-Ranin, Nevena and Stojić-Vukanić, Zorica and Čolić, Miodrag",
year = "2005",
abstract = "Fusidic acid and its sodium salt sodium fusidate (fusidin) are widely used antibiotics that possess immunomodulating properties. It has been shown that fusidin ameliorates the course of several organ-specific immunoinflammatory diseases and thus we investigated the effect of fusidin on myosin-induced experimental autoimmune myocarditis (EAM) in rats, a well-established animal model for human giant cell myocarditis and postmyocarditis dilated cardiomyopathy (DCM). Fusidin at doses of 80 mg kg(-1) was administrated i.m. to male Dark Agouti (DA) rats, either from days 0 to 10 (early treatment group), or from days 10 to 20 (late treatment group) after induction of EAM. Efficacy of fusidin treatment was determined on day 21 of EAM development. It was observed that both early and late treatment with fusidin markedly ameliorated clinical, histological and immunohistochemical signs of the disease. The treated rats had significantly decreased incidence of EAM, heart weight and heart weight/body weight ratio (Hw/Bw) compared with untreated animals. In contrast to the severe myocardial damage and cellular infiltration in the EAM rats, there was only focal infiltration of inflammatory cells in the myocardium of the treated rats. In both treated groups the mean microscopic score was markedly lower compared with vehicle-treated animals. In addition, the number of CD4+, ED1+ and OX6+ cells was significantly lower in myocardium of fusidin-treated rats than that in untreated group. The present findings suggest that fusidin exhibited both early and late therapeutical effect in EAM.",
publisher = "Academic Press Ltd- Elsevier Science Ltd, London",
journal = "Pharmacological Research",
title = "Suppression of experimental autoimmune myocarditis by sodium fusidate (fusidin)",
volume = "52",
number = "6",
pages = "491-496",
doi = "10.1016/j.phrs.2005.08.001"
}
Milenković, M., Vučićević, D., Milosavljević, P., Arsenović-Ranin, N., Stojić-Vukanić, Z.,& Čolić, M.. (2005). Suppression of experimental autoimmune myocarditis by sodium fusidate (fusidin). in Pharmacological Research
Academic Press Ltd- Elsevier Science Ltd, London., 52(6), 491-496.
https://doi.org/10.1016/j.phrs.2005.08.001
Milenković M, Vučićević D, Milosavljević P, Arsenović-Ranin N, Stojić-Vukanić Z, Čolić M. Suppression of experimental autoimmune myocarditis by sodium fusidate (fusidin). in Pharmacological Research. 2005;52(6):491-496.
doi:10.1016/j.phrs.2005.08.001 .
Milenković, Marina, Vučićević, Dragana, Milosavljević, P, Arsenović-Ranin, Nevena, Stojić-Vukanić, Zorica, Čolić, Miodrag, "Suppression of experimental autoimmune myocarditis by sodium fusidate (fusidin)" in Pharmacological Research, 52, no. 6 (2005):491-496,
https://doi.org/10.1016/j.phrs.2005.08.001 . .
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Beneficial effects of leflunomide on cardiac myosin-induced experimental autoimmune myocarditis in rats

Dimitrijević, Miroslava; Milenković, Marina; Milosavljević, P; Stojić-Vukanić, Zorica; Colić, M; Bartlett, R

(Bioscience Ediprint Inc, Carouge, 1998)

TY  - JOUR
AU  - Dimitrijević, Miroslava
AU  - Milenković, Marina
AU  - Milosavljević, P
AU  - Stojić-Vukanić, Zorica
AU  - Colić, M
AU  - Bartlett, R
PY  - 1998
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/186
AB  - The protective and therapeutical potential of a novel immunomodulatory agent, leflunomide, has been demonstrated in several experimental models of autoimmunity reactions leading to transplant rejection, as well as the therapy of patients with rheumatoid arthritis. in this study, the effects of leflunomide on experimentally induced autoimmune myocarditis (EAM) were investigated. Genetically susceptible DA rats were immunized with porcine cardiac myosin in complete Freund's adjuvant. The course of the disease was examined (on day 8, 16, 21 and 34) by macroscopic and microscopic scoring, heart weight/body weight ratio was determined and immunohistochemical analysis of inflammatory cell infiltrates was conducted. Eight days after disease induction, only slightly elevated expression of adhesive molecules on the interstitial and vascular endothelial cells were observed otherwise no microscopic signs of the inflammation existed. On day 16, numerous inflammatory cells infiltrated the myocardium. By day 21, the severity of myocarditis was substantially increased and was accompanied by extensive necrosis. After 34 days, decreased number of infiltrated cells was detected together with myocardial necrosis. Effects of leflunomide were evaluated by two treatment protocols. Rats immunized with cardiac myosin were injected i.p. with leflunomide's active metabolite, A 771726, at a dose of 10 mg/kg/day either during the first 6 days, or starting from day 14 and ending a: day 20 after disease induction. Efficacy of leflunomide treatment was determined on day 21 of EAM development Results demonstrated that early leflunomide treatment inhibited the inflammatory reaction, while late treatment significantly reduced EAM progression. Leflunomide may be considered a potent therapeutical tool for autoimmune myocarditis.
PB  - Bioscience Ediprint Inc, Carouge
T2  - International Journal of Immunotherapy
T1  - Beneficial effects of leflunomide on cardiac myosin-induced experimental autoimmune myocarditis in rats
VL  - 14
IS  - 1
SP  - 9
EP  - 21
UR  - https://hdl.handle.net/21.15107/rcub_farfar_186
ER  - 
@article{
author = "Dimitrijević, Miroslava and Milenković, Marina and Milosavljević, P and Stojić-Vukanić, Zorica and Colić, M and Bartlett, R",
year = "1998",
abstract = "The protective and therapeutical potential of a novel immunomodulatory agent, leflunomide, has been demonstrated in several experimental models of autoimmunity reactions leading to transplant rejection, as well as the therapy of patients with rheumatoid arthritis. in this study, the effects of leflunomide on experimentally induced autoimmune myocarditis (EAM) were investigated. Genetically susceptible DA rats were immunized with porcine cardiac myosin in complete Freund's adjuvant. The course of the disease was examined (on day 8, 16, 21 and 34) by macroscopic and microscopic scoring, heart weight/body weight ratio was determined and immunohistochemical analysis of inflammatory cell infiltrates was conducted. Eight days after disease induction, only slightly elevated expression of adhesive molecules on the interstitial and vascular endothelial cells were observed otherwise no microscopic signs of the inflammation existed. On day 16, numerous inflammatory cells infiltrated the myocardium. By day 21, the severity of myocarditis was substantially increased and was accompanied by extensive necrosis. After 34 days, decreased number of infiltrated cells was detected together with myocardial necrosis. Effects of leflunomide were evaluated by two treatment protocols. Rats immunized with cardiac myosin were injected i.p. with leflunomide's active metabolite, A 771726, at a dose of 10 mg/kg/day either during the first 6 days, or starting from day 14 and ending a: day 20 after disease induction. Efficacy of leflunomide treatment was determined on day 21 of EAM development Results demonstrated that early leflunomide treatment inhibited the inflammatory reaction, while late treatment significantly reduced EAM progression. Leflunomide may be considered a potent therapeutical tool for autoimmune myocarditis.",
publisher = "Bioscience Ediprint Inc, Carouge",
journal = "International Journal of Immunotherapy",
title = "Beneficial effects of leflunomide on cardiac myosin-induced experimental autoimmune myocarditis in rats",
volume = "14",
number = "1",
pages = "9-21",
url = "https://hdl.handle.net/21.15107/rcub_farfar_186"
}
Dimitrijević, M., Milenković, M., Milosavljević, P., Stojić-Vukanić, Z., Colić, M.,& Bartlett, R.. (1998). Beneficial effects of leflunomide on cardiac myosin-induced experimental autoimmune myocarditis in rats. in International Journal of Immunotherapy
Bioscience Ediprint Inc, Carouge., 14(1), 9-21.
https://hdl.handle.net/21.15107/rcub_farfar_186
Dimitrijević M, Milenković M, Milosavljević P, Stojić-Vukanić Z, Colić M, Bartlett R. Beneficial effects of leflunomide on cardiac myosin-induced experimental autoimmune myocarditis in rats. in International Journal of Immunotherapy. 1998;14(1):9-21.
https://hdl.handle.net/21.15107/rcub_farfar_186 .
Dimitrijević, Miroslava, Milenković, Marina, Milosavljević, P, Stojić-Vukanić, Zorica, Colić, M, Bartlett, R, "Beneficial effects of leflunomide on cardiac myosin-induced experimental autoimmune myocarditis in rats" in International Journal of Immunotherapy, 14, no. 1 (1998):9-21,
https://hdl.handle.net/21.15107/rcub_farfar_186 .
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