Suppression of experimental autoimmune myocarditis by sodium fusidate (fusidin)
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2005
Authors
Milenković, MarinaVučićević, Dragana
Milosavljević, P
Arsenović-Ranin, Nevena
Stojić-Vukanić, Zorica
Čolić, Miodrag
Article (Published version)
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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.
Keywords:
cardiac myosin / autoimmune myocarditis / sodium fusidate (fusidin)Source:
Pharmacological Research, 2005, 52, 6, 491-496Publisher:
- Academic Press Ltd- Elsevier Science Ltd, London
DOI: 10.1016/j.phrs.2005.08.001
ISSN: 1043-6618
PubMed: 16216521
WoS: 000233373900007
Scopus: 2-s2.0-27644545939
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PharmacyTY - 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 . .