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目的:观察硫化氢对大鼠急性心肌缺血组织细胞凋亡的影响及其作用机制。方法:健康雄性SD大鼠,随机分成7组:假手术组;心肌缺血组;心肌缺血+Na HS低剂量组;心肌缺血+Na HS中剂量组;心肌缺血+Na HS高剂量组;心肌缺血+SB216763组;心肌缺血+1%DMSO组。结扎大鼠冠状动脉左前降支复制急性心肌缺血模型。记录各组大鼠MAP、LVDP、LVEDP、dp/dt_(max)和dp/dt_(min),测定LDH活性、心肌细胞凋亡率、p-GSK-3β、t-GSK-3β、β-catenin、Bax和Bcl-2蛋白表达以及心肌组织形态学变化。结果:大鼠心肌缺血后MAP、LVDP、dp/dt_(max)和dp/dt_(min)降低,LVEDP升高,血清LDH活性增强,心肌细胞凋亡率和Bax表达增强,Bcl-2表达降低,p-GSK-3β、p-GSK-3β/t-GSK-3β和β-catenin表达降低。心肌纤维横纹不齐或消失,核偏移甚至裂解消失。给予Na HS后,大鼠MAP、LVDP、dp/dt_(max)和dp/dt_(min)均升高,LVEDP降低,血清LDH活性降低,心肌细胞凋亡率和Bax表达降低,Bcl-2表达增强,心肌p-GSK-3β、p-GSK-3β/t-GSK-3β和β-catenin表达均增强,心肌细胞变性程度明显减轻。结论:硫化氢可通过GSK-3β/β-catenin信号途径介导心肌损伤后抗细胞凋亡作用。
Objective: To observe the effect of hydrogen sulfide on apoptosis of acute myocardial ischemia in rats and its mechanism. Methods: Healthy male Sprague-Dawley rats were randomly divided into 7 groups: sham operation group, myocardial ischemia group, myocardial ischemia + Na HS low dose group, myocardial ischemia + Na HS medium dose group, myocardial ischemia + Na HS high dose Group; myocardial ischemia + SB216763 group; myocardial ischemia + 1% DMSO group. Ligation of left anterior descending coronary artery in rats with acute myocardial ischemia model. The MAP, LVDP, LVEDP, dp / dt max and dp / dt min were recorded and the activities of LDH, the apoptosis rate of cardiomyocytes, the expressions of p-GSK-3β, t-GSK-3β and β-catenin , Bax and Bcl-2 protein expression and myocardial tissue morphological changes. Results: After myocardial ischemia, MAP, LVDP, dp / dt max and dp / dt min decreased, LVEDP increased, serum LDH activity increased, myocardial cell apoptosis rate and Bax expression increased, Bcl- Decreased the expression of p-GSK-3β, p-GSK-3β / t-GSK-3β and β-catenin. Abnormal or disorganized myocardial fibers, nuclear shift or even disappear. After Na HS administration, MAP, LVDP, dp / dt max and dp / dt min increased, LVEDP decreased, serum LDH activity decreased, cardiomyocyte apoptosis rate and Bax decreased, Bcl-2 expression The expression of p-GSK-3β, p-GSK-3β / t-GSK-3βand β-catenin in myocardium were increased and the degree of myocardial cell degeneration was significantly reduced. Conclusion: Hydrogen sulfide can mediate anti-apoptotic effect after myocardial injury through GSK-3β / β-catenin signaling pathway.