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Suppression of experimental autoimmune myocarditis by sodium fusidate (fusidin)

Samo za registrovane korisnike
2005
Autori
Milenković, Marina
Vučićević, Dragana
Milosavljević, P
Arsenović-Ranin, Nevena
Stojić-Vukanić, Zorica
Čolić, Miodrag
Članak u časopisu (Objavljena verzija)
Metapodaci
Prikaz svih podataka o dokumentu
Apstrakt
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.

Ključne reči:
cardiac myosin / autoimmune myocarditis / sodium fusidate (fusidin)
Izvor:
Pharmacological Research, 2005, 52, 6, 491-496
Izdavač:
  • 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
[ Google Scholar ]
7
6
URI
http://farfar.pharmacy.bg.ac.rs/handle/123456789/595
Kolekcije
  • Radovi istraživača / Researchers’ publications
Institucija
Pharmacy

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