In the present study, we investigated the potential pathogenesis of coxsackievirus B3 (CVB3)-induced viral
myocarditis and the promising protective effect of silencing
RNA (small interfering RNA,
siRNA). One hundred and twenty mice were included in the study, and 30 mice were intraperitoneally inoculated with CVB3 to establish an acute viral
myocarditis model. The survival rate was observed for the CVB3-infected mouse model (MOD), and myocardial injury was examined by HE (
hematoxylin and
eosin) staining assay. Real-time PCR (RT-PCR) and Western blot assay were selected to detect the
toll-like receptor 4 (TLR4) expression in myocardial tissues. The TLR4 gene was silenced for the MOD mice, and the effects of this treatment were observed. The results indicate that the expression of TLR4
mRNA and the
protein significantly and persistently increased during the progression of CVB3-induced
myocarditis. The activities of cardiac
enzymes including CK, LDH, AST, and CK-MB were also enhanced in CVB3-induced myocardial tissues. Interestingly, when the TLR4 gene was silenced, the CVB3-induced TLR4 production was significantly decreased and the severity of
myocarditis was significantly lessened. In conclusion, CVB3 may induce viral
myocarditis by upregulating
toll-like receptor 4 expression. The viral
myocarditis can be ameliorated by silencing the TLR4 gene in the CVB3 viral
myocarditis model, which may be a feasible therapeutic method for treatment of viral
myocarditis.