尼可地尔后处理对急性缺血诱导的大鼠心肌细胞凋亡的影响

目的 探讨尼可地尔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 SD大鼠随机分为6组:假手术组、缺血再灌注组、缺血后处理组、尼可地尔后处理2、5和10 mg/kg剂量组.采用左冠状动脉前降支结扎30 min、再灌注120 min建立大鼠心肌缺血再灌注模型.缺血后处理组在缺血后再灌注前实施5次10 s再灌注-10 s再阻断循环.尼可地尔后处理组在缺血后再灌注前分别给予三个剂量10 min.检测血清肌酸激酶和丙二醛含量,及超氧化物歧化酶活性;检测心肌细胞的凋亡率和Caspase-3蛋白的表达.结果 尼可地尔后处理能使肌酸激酶、丙二醛含量降低,超氧化物歧化酶活性增高,心肌细胞凋亡率降低, Caspase-3蛋白表达减少.结论 尼可地尔后处理对缺血再灌注损伤的心肌具有保护作用,其机制可能与提高超氧化物歧化酶活性,增强心肌抗氧化能力,减轻氧自由基损伤,稳定细胞膜,抑制细胞凋亡有关.

The Effects of Nicorandil Postconditioning on Ischemia-Induced Cardiomyocyte Apo-tosis in Acute Myocardial Ischemia Rats

Aim To study the effect and possiblemechanism of nicorandil postconditioning on myocardial ische-mia reperfusion (MIR) injury in rats.Methods The SD rats were randomly divided into six groups: control group,ischemia reperfusion group, postconditioning group, nicorandil postconditioning groups of 2 mg/kg, 5 mg/kg, and 10 mg/kg.Ischemia reperfusion group was obtained by ligated left anterior descending coronary artery 30 minutes and followed by 120 minutes reperfusion.Postconditioning group was obtained by 5 cycles of brief 10 seconds intermittent reperfusion/re-occlusion.After 30 minutes ischemia, hearts were exposed to nicorandil for 10 minutes immediately at the onset of reper-fusion.Contents of creatine kinase (CK) and malondialdehyde (MDA), activity of superoxide dismutase (SOD) were detected respectively.Apoptosis rates and the expression of caspase-3 were investigated.Results In the nicorandil postconditioning groups, contents of CK and MDA were lower, activities of SOD were higher, apotosis rates were de-creased, and caspase-3 was lower.Conclusions Nicorandil postconditioning could protect MIR.The myocardial protective mechanism maybe realized by enhancing the activity of SOD, enhancing myocardial antioxygen capability, reduc-ing the oxygen free radical injury, stabilizing myocardial cellularmembrance and inhibition of apoptosis.