心肌远隔缺血预适应通过SDF-1α/CXCR4途径保护兔心肌缺血/再灌注损伤的研究

摘要

目的:探讨远隔缺血预适应对心肌缺血/再灌注(I/R)损伤保护作用及潜在机制.方法:成年雄性新西兰大白兔随机分成:①心肌缺血再灌注组(I/R组,n=6);②假手术组(Sham,n=6);③远隔缺血预适应(RIPC+I/R组,n=6);④SDF-1 α/CXCR4阻断剂AMD3100+I/R组,(n=6);⑤AMD3100+RIPC+UR组,(n=6).ELISA检测外周血中SDF-lα;TTC检测心肌梗死面积;TUNEL检测细胞凋亡率;Western Blot检测Bcl-2、Bax蛋白表达.结果:与Sham组相比,I/R组及RIPC+I/R组都可促进外周血中SDF-1α的释放,且后者的作用更显著(P＜0.05);RIPC+I/R及AMD3100+RIPC+UR组可以不同程度缩小心肌梗死面积及降低心肌细胞凋亡率(P＜0.05),AMD3100+RIPC+I/R组与RIPC+I/R组相比,心肌梗死面积及细胞凋亡率均有所增加(P＜0.05).结论:远隔缺血预适应可能通过SDF-1 αt/CXCR4信号通路对心缺血再灌注损伤心肌发挥保护作用.%Objective:To investigate the protective effect of remote ischemic preconditioning(PIPC) on myocardial ischemia/reperfusion(I/R) injury and underlying mechanism.Method:Clean level male white rabbits of New Zealand,weight 2.2-2.5 kg,were randomly divided into the following groups:Sham (n=6),myocardial I/R(n=6),RIPC+I/R (n=6),SDF-1α/CXCR4 inhibitor(AMD3100)+I/R,AMD3100+RIPC+I/R.The release of SDF-1αt was detected by ELISA from the serum,the size of myocardial infarction was assayed by TTC,cardiomyocyte apoptosis rate was detected by TUNEL,and the expressions of Bcl-2,Bax were assessed via western blot.Result:Myocardial I/R and RIPC+I/R can promote the expressions of SDF-1α compared with Sham group(P＜0.05),more obvious in RIPC+I/R group(P＜0.05);Compared with I/R group,myocardium infarction area and cardiomyocyte apoptosis rate were reduced between RIPC+I/R and AMD3100+RIPC+I/R,with the increase of Bcl-2,the decrease of Bax(P＜0.05).By comparing with RIPC+I/R group,myocardium infarction area and cardiomyocyte apoptosis rate were increased in AMD3100+RIPC+I/R group(P＜0.05).Conclusion:RIPC can promote SDF-1α release to exert the cardioprotection effect against myocardium iscbemia reperfusion injury via SDF-1α/CXCR4 signal pathway.