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目的:观察乙酰半胱氨酸对糖尿病大鼠心肌缺血/再灌注后导致的细胞凋亡的影响,探讨其机制。方法:链尿佐菌素诱导糖尿病大鼠模型,随机分为假手术组、缺血/再灌注组和缺血/再灌注+乙酰半胱氨酸治疗组。组织匀浆检测心肌组织还原型谷胱甘肽(GSH)、氧化型谷胱甘肽(GSSG)含量和半胱氨酸天冬氨酸蛋白酶-3(Caspase-3)的活性;脱氧核糖核苷酸末端转移酶介导的缺口末端标记(TUNEL)和琼脂糖凝胶电泳检测DNA片段化两种方法检测心肌细胞凋亡并计算凋亡指数。结果:缺血/再灌注后,糖尿病和非糖尿病组均出现明显的心肌细胞凋亡,同时伴有GSH含量降低,GSSG含量和Caspase-3的活性升高,上述变化糖尿病组比非糖尿病组更明显(P<0.05);乙酰半胱氨酸干预的糖尿病和非糖尿病大鼠的心肌细胞凋亡均减轻,同时伴有GSH含量上升,GSSG含量和Caspase-3的活性下降,上述变化非糖尿病组比糖尿病组更明显(P<0.05)。结论:乙酰半胱氨酸干预可以通过提高心肌GSH含量、降低Caspase-3的活性减轻糖尿病和非糖尿病大鼠缺血/再灌注引起的心肌细胞凋亡,对缺血/再灌注心肌有保护作用,但糖尿病组的疗效低于非糖尿病组。
Objective: To investigate the effect of acetylcysteine on apoptosis induced by myocardial ischemia / reperfusion in diabetic rats and its mechanism. Methods: Streptozotocin-induced diabetic rat models were randomly divided into sham operation group, ischemia / reperfusion group and ischemia / reperfusion + acetylcysteine treatment group. The contents of reduced glutathione (GSH), oxidized glutathione (GSSG) and caspase-3 in myocardium were detected by histological homogenization. The activity of deoxyribonucleoside TUNEL and agarose gel electrophoresis were used to detect cardiomyocyte apoptosis and calculate apoptotic index. Results: After ischemia / reperfusion, both cardiomyocytes and non-diabetic rats showed obvious cardiomyocyte apoptosis accompanied by decreased GSH content and GSSG content and Caspase-3 activity. Compared with non-diabetic patients (P <0.05) .Apoptosis of myocardial cells in both diabetic and non-diabetic rats was alleviated by acetylcysteine accompanied by an increase in GSH content and a decrease in GSSG content and Caspase-3 activity in the non-diabetic group More obvious than the diabetic group (P <0.05). CONCLUSION: Acetylcysteine can protect myocardium from ischemia / reperfusion injury by increasing GSH content and decreasing Caspase-3 activity in myocardium of ischemia and reperfusion-induced diabetic rats and non-diabetic rats , But the efficacy of diabetic group than non-diabetic group.