凋亡相关蛋白在曲美他嗪干预的心力衰竭大鼠心肌细胞中的表达

Expression of apoptotic associated proteins in myocardial cells of heart failure rat intervented by trimetazidine

目的：探讨曲美他嗪对心力衰竭心肌细胞凋亡情况及Bax、Bcl-2蛋白表达的影响.方法：随机将雄性Wistar大鼠分为假手术组、心衰组和曲美他嗪组,除假手术组其他组大鼠均采用腹主动脉缩窄术建立心衰模型.观察各组大鼠的血流动力学参数,H-E染色观察大鼠心肌细胞病理形态结构,透射电镜观察心肌细胞超微结构,原位缺口末端标记（TUNEL）法检测心肌细胞凋亡指数（AI）;免疫组织化学检测各组大鼠心肌细胞Bax、Bcl-2蛋白的表达情况.结果：与模型组比较,曲美他嗪组大鼠心功能明显改善,AI明显降低,Bcl-2阳性表达显著增高,Bax阳性表达明显降低.结论：曲美他嗪可促进抑凋亡蛋白Bcl-2的表达,抑制促凋亡蛋白Bax的表达,该机制可能参与了曲美他嗪的心保护作用.

Objective：To investigate the effect of trimetazidine on apoptosis and expression of apoptosis-related protein Bax and Bcl-2 in rats with chronic heart failure.Methods：Male Wistar rats were randomly divided into a sham-operated group,a heart failure group,a trimetazidine group.In addition to the sham-operated group,chronic heart failure model was established in the other groups by suprarenal aortic constriction.The hemodynamic parameters were measured.H-E staining was used to observe the morphology of myocardium.The myocardial ultrastructure was observed by transmission electronic microscopy.The apoptotic index （AI） of myocardium was detected by terminal-deoxynucleoitidyl transferase mediated dUTP nick end abeling （TUNEL） assay.The expressions of Bax and Bcl-2 were evaluated by immunohistochemistry assay.Results：The heart function was significantly better and the expression levels of Bcl-2 protein were significantly higher,while AI and the expression levels of Bax protein were significantly lower in the trimetazidine group,than those in the model group.Conclusion：The expression of pro-apoptotic protein Bax could be reduced,while the expression of anti-apoptotic protein Bcl-2 could be increased in chronic heart failure rats by trimetazidine.The inhibitory effect of trimetazidine on myocardium apoptosis may play an important role in the cardial protection.