缺血后处理对缺血再灌注大鼠心脏凋亡相关酶活性的影响

目的 观察缺血后处理对大鼠心肌缺血再灌注造成细胞凋亡及凋亡相关酶活性的影响。方法 采用冠状动脉左前降支结扎法制备大鼠心肌缺血再灌注模型,HE染色观察心肌组织病理学改变,TUNEL法检测大鼠心肌细胞凋亡水平,比色法检测心肌组织总抗氧化能力(TAOC)、丙二醛(MDA)水平,分光光度法检测心肌组织Caspase-3、Caspase-9活性。结果 缺血再灌注造成大鼠心肌组织抗氧化能力明显降低(P＜0.01),心肌细胞凋亡明显增加(P＜0.01),Caspase-3、Caspase-9酶活性以及MDA水平明显升高(P＜0.01),缺血后处理能够改善上述表现(P＜0.05)。结论 缺血后处理可通过抑制凋亡相关蛋白酶活性减轻缺血再灌注造成的大鼠心肌细胞损伤。

Effect of ischemic postconditioning on apoptosis associated enzymes in myocardial ischemia reperfusion rats

Objective To observe the effect of ischemic postconditioning on myocardial apoptosis and enzymes associated with apoptosis in myocardial ischemia reperfusion rats. Methods Ischemia reperfusion model of rat was established by left anterior descending coronary artery ligation. The primary pathologic change was observed by HE staining; Myocardial apoptosis rate was observed by TUNEL assay; Total antioxidant capacity (T-AOC) and malondialdehyde (MDA) level in cardiac tissue were measured by colorimetric assay. Activities of Caspase-3 and Caspase-9 were detected by spectrophotometric method. Results The antioxidant capacity of myocardial tissue in ischemia reperfusion rats was obviously lower than that in sham-operated rats. Level of MDA, activities of Caspase-3 and Caspase-9 as well as cell apoptosis were much higher in ischemia reperfusion rats than those in sham-operated rats. Ischemic postconditioning could improve detection indexes above obviously. Conclusion Ischemic postconditioning can protect ischemia reperfusion rat from myocardial cell injury by inhibiting activities of Caspase-3, Caspase-9 and myocardial apoptosis.