| Objective This study was designed to explore the mechanismof fenofibrate treated on EAM rats.Methods experimental autoimmunemyocarditis (EAM) rats were injected with porcine cardiac myosin andcomplete Freund’s adjuvant in double feet.Fenofibrate(100mg/kg/d)orvehic was administered orally from D0to D17, while physiological salinewas administered orally from D0to D17On EAM group. On day17, Cardiacfunction was examined by echocardiography and the severity of myocarditiswas evaluated by hematoxylin and eosin (HE) staining. the mRNA expressionof Atrium natriuretic peptide (ANP)and brain natriuretic peptide(BNP)，Th1-type cytokines (IFN-γ,IL-2)and Th2-type cytokines(IL-4,IL-10) weredetermined by Quantative RT-PCR,and the serum level of IFN-γ,IL-4weremeasured by ELISA.Results The relative expression of Atrium natriureticpeptide (ANP)and brain natriuretic peptide(BNP) were elevated in EAMgroup but decressed in fenofibrate group Compared to EAM group,the cardiacfunction was improved in Fenofibrate treated group.Heart weight/bodyweight and the degree of inflammation in heart were significantly lowerin fenofibrate treated group than that in EAM group.In addition,treatmentwith fenofibrate decreased the expression of Th1-type cytokines(IFN-γ，IL-2) and increased the expression of Th2-type cytokines (IL-4,IL-10).Conclusions Fenofibrate may ameliorate EAM through modulating the balanceof Th1/Th2cytokine. |
PDF Full Text Request