Original Article
Total Astragalus saponins attenuates CVB3-induced viral myocarditis through inhibiting expression of tumor necrosis factor α and Fas ligand
Abstract
Background: To investigate the therapeutic effect of total Astragalus saponins (AST) against viral myocarditis in animal and cell models.
Methods: Primary myocardiocytes (PMCs) were stimulated by the coxsackie B (CVB) 3 virus to prepare the cell model of viral myocarditis. Cell viability, apoptosis and the mRNA expression of C-Myc, tumor necrosis factor (TNF)-α and Fas were detected to evaluate the protective effects of AST on CVB3-induced PMC damage.
Results: AST could significantly increase survival and decrease the ratio of heart weight: body weight (P<0.05). The level of myocardial brosis in the AST group was signi cantly lower than that in the CVB3 group. Compared with the CVB3 group, the ejection fraction was increased signi cantly in the AST group. Levels of lactate dehydrogenase and creatine kinase-MB in the peripheral blood of the AST group were significantly lower than those in the control group. In vitro, AST could significantly decrease CVB3-induced PMC apoptosis. Expression of C-Myc, TNF-α, Fas in the AST group was significantly lower than that in the CVB3 group.
Conclusions: It is demonstrated that AST was protective against CVB3-induced viral myocarditis, which may be associated with a decrease in CVB3-induced apoptosis and down-regulation of expression of C-Myc, TNF-α and Fas.
Methods: Primary myocardiocytes (PMCs) were stimulated by the coxsackie B (CVB) 3 virus to prepare the cell model of viral myocarditis. Cell viability, apoptosis and the mRNA expression of C-Myc, tumor necrosis factor (TNF)-α and Fas were detected to evaluate the protective effects of AST on CVB3-induced PMC damage.
Results: AST could significantly increase survival and decrease the ratio of heart weight: body weight (P<0.05). The level of myocardial brosis in the AST group was signi cantly lower than that in the CVB3 group. Compared with the CVB3 group, the ejection fraction was increased signi cantly in the AST group. Levels of lactate dehydrogenase and creatine kinase-MB in the peripheral blood of the AST group were significantly lower than those in the control group. In vitro, AST could significantly decrease CVB3-induced PMC apoptosis. Expression of C-Myc, TNF-α, Fas in the AST group was significantly lower than that in the CVB3 group.
Conclusions: It is demonstrated that AST was protective against CVB3-induced viral myocarditis, which may be associated with a decrease in CVB3-induced apoptosis and down-regulation of expression of C-Myc, TNF-α and Fas.
