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目的 探讨心肌细胞凋亡在充血性心力衰竭 (CHF)发生、发展中的作用 ,Bcl 2和Fas及其配体 (FasL)对心肌细胞凋亡的调控机制。方法 采用心肌梗死 (MI)大鼠模型 ,观察雄性Wistar大鼠MI后 2、4及 8周的血流动力学参数、心室重塑指标、心肌细胞凋亡、Fas、FasL和Bcl 2的mRNA和蛋白表达的改变。结果 MI后 4周大鼠出现平均动脉压、±dp dtmax下降 ,左室舒张末压、右室 体重比增高 ,MI后 8周上述改变更为明显 ;MI后心肌细胞凋亡指数、Fas及FasL的mRNA和蛋白表达逐渐升高 ,Bcl 2的mRNA和蛋白表达下调。结论 心肌细胞凋亡在MI后CHF发生、发展过程中起着重要的作用 ,Fas和FasL表达上调、Bcl 2表达下降介导MI后心肌细胞凋亡的发生。
Objective To investigate the role of cardiomyocyte apoptosis in the development and progression of congestive heart failure (CHF) and the regulatory mechanism of apoptosis induced by Bcl 2, Fas and its ligand (FasL). Methods The myocardial hemodynamic parameters, ventricular remodeling, cardiomyocyte apoptosis, mRNA expression of Fas, FasL and Bcl 2 in male Wistar rats at 2, 4 and 8 weeks after myocardial infarction (MI) were observed. Changes in protein expression. Results The mean arterial pressure, ± dp dtmax, left ventricular end-diastolic pressure, and right ventricular mass ratio were increased 4 weeks after MI in MI rats. These changes were more obvious at 8 weeks after MI. The apoptosis index, Fas and FasL MRNA and protein expression gradually increased, Bcl 2 mRNA and protein expression down. Conclusions Cardiomyocyte apoptosis plays an important role in the development of CHF after MI. Fas and FasL are up-regulated and Bcl-2 is down-regulated in cardiomyocytes.