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目的:探讨血管紧张素转化酶抑制剂(ACEI)———依那普利对慢性压力负荷性心力衰竭大鼠心肌重构、心肌细胞凋亡、凋亡基因Bcl 2、Bax在心肌细胞中表达的影响,为心力衰竭的发病机制及治疗提供实验依据。方法:结扎大鼠的腹主动脉,复制慢性压力负荷性心力衰竭模型,32只大鼠随机分为心力衰竭组 12 只、依那普利治疗组(治疗组)12只、对照组8只。手术后6周,充血性心力衰竭模型形成。治疗组给予依那普利10 mg·kg-1·d-1灌胃,心力衰竭组和对照组给予同量0.85%氯化钠溶液灌胃。在 3 个月末测量血流动力学指标后,将大鼠处死,取出心脏。用原位脱氧核糖核酸酶末端标记法(TUNEL)检测细胞凋亡;免疫组化法和免疫印迹法测 bcl 2、Bax表达。结果:心力衰竭组与对照组相比,心功能明显减退(P < 0.01);心肌细胞凋亡明显增加(P <0.01);在心肌细胞中bcl 2 表达减低,Bax表达增加。依那普利治疗后能改善心室重构(P<0.05),减少心肌细胞凋亡(P< 0.01),增加bcl 2、减少Bax在心肌细胞中的表达(P<0.05)。结论:在心力衰竭时血管紧张素Ⅱ生成增多,减低bcl 2的表达,增加Bax的表达,从而降低 bcl 2/Bax比率;依那普利可能通过血管紧张素Ⅱ的介导作用,增加bcl 2、减低Bax在心肌细胞中的表达,减轻心肌细胞凋亡。
AIM: To investigate the effects of enalapril on myocardial remodeling, cardiomyocyte apoptosis, expression of Bcl-2 and Bax in cardiomyocytes in rats with chronic pressure overload heart failure Of the impact of heart failure for the pathogenesis and treatment to provide experimental evidence. Methods: The abdominal aorta of rats were ligated and the chronic stress-loaded heart failure model was duplicated. Thirty-two rats were randomly divided into 12 groups of heart failure, 12 of enalapril treatment group (treatment group) and 8 of control group. Six weeks after surgery, a congestive heart failure model was established. The treatment group was given enalapril 10 mg · kg -1 · d -1 intragastrically, and the heart failure group and the control group were given the same amount of 0.85% sodium chloride solution. After measuring hemodynamic parameters at the end of 3 months, the rats were sacrificed and the heart removed. Apoptosis was detected by in situ deoxyribonuclease end labeling (TUNEL), and the expressions of bcl 2 and Bax were detected by immunohistochemistry and Western blot. Results: Compared with the control group, heart failure decreased significantly (P <0.01), cardiomyocyte apoptosis increased significantly (P <0.01), decreased expression of bcl 2 and increased expression of Bax in cardiomyocytes. Enalapril treatment could improve ventricular remodeling (P <0.05), decrease cardiomyocyte apoptosis (P <0.01), increase bcl 2 and decrease Bax expression in cardiomyocytes (P <0.05). CONCLUSION: Angiotensin II production is increased, the expression of bcl 2 is reduced, the expression of Bax is increased and the ratio of bcl 2 / Bax is decreased in heart failure. Enalapril may increase bcl 2 through the mediation of angiotensin Ⅱ , Reduce the expression of Bax in cardiomyocytes and reduce the cardiomyocyte apoptosis.