摘要
目的观察缺血后处理对大鼠心肌缺血再灌注中心肌细胞凋亡的影响并探讨其机制。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,TUNEL法检测大鼠心肌细胞凋亡水平,比色法检测血清LDH及NO水平,免疫组化法检测心肌细胞iNOS蛋白表达水平。结果缺血再灌注造成大鼠心肌细胞LDH释放及凋亡明显增加,缺血后处理明显减少LDH释放及心肌细胞凋亡,同时增加iNOS蛋白表达及NO合成。结论缺血后处理对缺血再灌注大鼠心肌细胞损伤具有保护作用,与增加iNOS蛋白表达及NO合成,抑制心肌细胞凋亡有关。
Objective To investigate the protect effect of ischemic post-conditioning on myocardial apoptosis in myocardial ischemia reperfusion rats and its mechanism.Methods Ischemia reperfusion model of rat was established by left anterior descending coronary artery ligation. Myocardial apoptosis rate was observed by TUNEL assay,levels of LDH and NO in serum were detected by colorimetric determination,iNOS protein expression was examined by immunohistochemical staining. Results LDH release and myocardial apoptosis were much higher in myocardial ischemia reperfusion rats than those in sham-operated rats. Ischemic post-conditioning could reduce LDH release and myocardial cell apoptosis obviously,accompanied by protein expression of iNOS and level of NO markedly increased. Conclusions Ischemic post-conditioning can protect ischemia reperfusion rat from myocardial cell injury. The potential mechanism may derived from expression of iNOS,the synthesis of NO,and inhibiting myocardial apoptosis.
出处
《齐齐哈尔医学院学报》
2017年第21期2493-2494,共2页
Journal of Qiqihar Medical University
基金
安徽省教育厅高等学校省级质量工程项目:医学影像技术专业实验实训中心(2016sxzx012)
安徽省教育厅高等职业教育创新发展行动计划(2015-2018)项目:医学影像技术专业双主体教学基地-池州市人民医院(XM-02)
关键词
缺血后处理
凋亡
一氧化氮合成酶
Ischemic post-conditioning
Apoptosis
Nitric oxide synthase