黄芪三萜皂苷对CVB3诱导病毒性心肌炎的保护作用研究

目的：研究黄芪三萜皂苷（Astragalus saponins，AST）对CVB3病毒诱导病毒性心肌炎的保护作用及机制。方法：利用CVB3病毒、原代心肌细胞及小鼠构建病毒性心肌炎模型并使用AST进行干预，在实验过程中记录小鼠的生存率和体质量变化，体外超声评价小鼠的心脏功能及检测心肌蛋白中LDH和CK-MB水平。心肌组织天狼星红染色评价纤维化水平及TUNNEL染色检测心肌凋亡情况。Western Blot检测心肌蛋白中Caspase-3和Fas表达情况以研究AST保护病毒性心肌炎的机制。结果：AST能够显著增加CVB3注射后的小鼠生存率、缓解CVB3诱导小鼠的体质量减轻。体外超声结果显示，AST能够显著改善CVB3诱导小鼠心脏的收缩功能障碍。CBV3诱导组小鼠心肌蛋白中LDH和CM-KB水平较正常小鼠显著增加，而AST对此有显著的抑制作用。心肌组织病理染色结果显示，AST对CVB3诱导的心肌扩张和纤维化具有显著的保护作用。CVB3诱导组小鼠心肌组织的凋亡水平显著高于正常小鼠，而AST对此有显著的抑制作用。在CVB3感染的心肌组织中，Caspase-3和Fas表达水平显著的升高，而AST能够显著的抑制CVB3诱导的二者在心肌组织中的表达。结论：AST通过提高小鼠的生存率、抑制心肌扩张、心肌组织纤维化和心肌细胞凋亡对CVB3诱导的病毒性心肌炎具有显著的保护作用，这种作用可能与抑制CVB3诱导的Caspase-3和Fas在心肌组织中表达有关。

The protective effect of AST on CVB3-induced viral myocarditis

OBJECTIVE To study the protective effect and mechanism of Astragalus saponins (AST) against viral myocarditis in mice.METHODS CVB3, cardiomyocytes and BALB/C mice were used to prepare mouse model of viral myocarditis, which was then treated with AST. The protective effects of AST were evaluated by survival, the ratio of heart to body weight, echocardiographic assessment, the extent of myocardial fibrosis, and the expression of LDH and CK-MB in peripheral blood. Cell viability, apoptosis and the mRNA expression of Caspase-3 and Fas were detected to evaluate the protective mechanism of AST on CVB3-induced myocarditis.RESULTS AST could significantly increase survival and decrease the ratio of heart to body weight. Myocardial fibrosis level in the AST group was significantly lower than that in the CVB3 group. Compared with the CVB3 group, the ejection fraction was increased significantly in the AST group. Levels of LDH and CK-MB in the heart were significantly lower in heart of AST treatment than those in the CVB3-induced heart. In vitro, AST could significantly decrease CVB3-induced primary cardiomyocytes apoptosis. Expressions of Caspase-3 and Fas in the AST group were significantly lower than those in the CVB3 group.CONCLUSION AST has a protective effect against CVB3-induced viral myocarditis, which may be associated with a decrease in CVB3-induced apoptosis and down-regulation of expression of Caspase-3 and Fas.