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目的探讨克罗卡林后处理对大鼠心肌缺血再灌注损伤的保护作用及机制。方法采用左冠状动脉前降支结扎30min再灌120min建立大鼠心肌缺血再灌注模型。SD大鼠随机分为5组:假手术组,缺血再灌注组,缺血后处理组,克罗卡林后处理组,克罗卡林后处理+线粒体ATP敏感性钾通道阻断剂5-HD组,每组8只。观察心肌病理结构改变,肌酸激酶活性、超氧化物歧化酶(SOD)活性、丙二醛含量、三磷酸腺苷(ATP)含量变化和凋亡抑制蛋白Bcl-2、凋亡蛋白Bax表达的变化。结果克罗卡林后处理能减轻心肌损伤程度,使SOD活性增高,丙二醛含量降低,ATP含量增高,Bcl-2蛋白表达增加,Bax蛋白表达减少。加入线粒体ATP敏感性钾通道阻断剂5-HD后以上保护作用被阻断。结论克罗卡林后处理可减少缺血再灌注心肌损伤,增强心肌抗氧化能力,减少细胞凋亡,这种保护作用与激活线粒体ATP敏感性钾通道密切相关。
Objective To investigate the protective effect and mechanism of crotaline postconditioning on myocardial ischemia-reperfusion injury in rats. Methods The left anterior descending coronary artery was ligated for 30 min and then reperfused for 120 min to establish a model of myocardial ischemia-reperfusion in rats. Sprague-Dawley rats were randomly divided into 5 groups: sham operation group, ischemia-reperfusion group, ischemic postconditioning group, post-treatment group of crotaline, post-treatment of mitochondria + mitochondrial ATP sensitive potassium channel blocker 5 -HD group, 8 in each group. The changes of cardiac pathology and structure, creatine kinase activity, superoxide dismutase (SOD) activity, malondialdehyde (MDA) content, ATP content, Bcl-2 and Bax expression were observed. Results The post-treatment with buprenorphine could reduce the degree of myocardial injury, increase SOD activity, decrease MDA content, increase ATP content, increase Bcl-2 protein expression, and decrease Bax protein expression. The above protective effect was blocked by adding mitochondrial ATP-sensitive potassium channel blocker 5-HD. Conclusions Chromarimine treatment can reduce myocardial ischemia-reperfusion injury, enhance myocardial antioxidant capacity and reduce apoptosis. This protective effect is closely related to the activation of mitochondrial ATP-sensitive potassium channels.