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目的探讨心肌梗死后心力衰竭大鼠心肌组织ACE/ACE2表达变化及苯钠普利的干预作用。方法结扎大鼠左冠状动脉前降支复制心肌梗死后心衰模型,分为心衰对照组、苯钠普利组、假手术组。喂养2个月后检测血流动力学指标,计算体重与左心室重量指数,RT-PCR方法检测心肌组织ACE和ACE2 mRNA表达,免疫组化检测ACE和ACE2蛋白表达。结果心衰对照组大鼠心肌组织ACE和ACE2的mRNA和蛋白表达均增强(P<0.01),ACE/ACE2比值升高。苯钠普利组大鼠血流动力学指标改善(P<0.01),心肌组织ACE mRNA和蛋白表达下降(P<0.01),ACE2 mRNA和蛋白表达显著增强(P<0.01),ACE/ACE2比值降低。结论心衰大鼠心肌组织ACE和ACE2表达上调,ACE上调更显著,ACE/ACE2比值升高;苯钠普利抑制ACE表达,刺激ACE2表达增强,ACE/ACE2比值下降,这是对该药物作用机制的新解释。
Objective To investigate the changes of myocardial ACE / ACE2 expression in rats with heart failure after myocardial infarction and the effect of preconcentration of sodium. Methods The left anterior descending coronary artery of rats was ligated to establish the model of heart failure after myocardial infarction. The model was divided into heart failure control group, benazapril group and sham operation group. Two months after feeding, hemodynamic parameters were measured to calculate body weight and left ventricular mass index. The expression of ACE and ACE2 mRNA in myocardium was detected by RT-PCR and the expressions of ACE and ACE2 were detected by immunohistochemistry. Results The mRNA and protein expressions of ACE and ACE2 were increased in the heart failure control group (P <0.01), and the ratio of ACE / ACE2 was increased. The hemodynamic indices of rats in the benapinil group were significantly improved (P <0.01), the levels of ACE mRNA and protein in the myocardium were decreased (P <0.01), and the mRNA and protein expressions of ACE2 were significantly increased (P <0.01) reduce. CONCLUSIONS: ACE and ACE2 are upregulated in cardiac tissue of rats with heart failure, with a significant increase of ACE and a higher ratio of ACE / ACE2. Benzoprolide inhibits the expression of ACE, stimulates the expression of ACE2 and decreases the ratio of ACE / ACE2 A new explanation of the mechanism.