硫化氢延迟预处理对大鼠心肌缺血再灌注损伤后细胞的保护作用  

Cytoprotection of hydrogen sulfide delayed preconditioning on myocardial ischemic reperfusion injury in rats

作　　者：李双凤[1] 冉珂[1] 王亚平[1] 唐正国 肖艳英[1] 王丹[1] 

机构地区：[1]中南大学湘雅二医院麻醉科,长沙410011 [2]长沙市第三医院麻醉科,长沙410011

出　　处：《郑州大学学报（医学版）》2011年第4期526-528,共3页Journal of Zhengzhou University(Medical Sciences)

基　　金：湖南省卫生厅基金资助项目B2009110

摘　　要：目的:观察硫化氢(H2S)延迟预处理对大鼠心肌缺血再灌注(IR)损伤后细胞的保护作用及可能机制。方法:雄性SD大鼠32只,分为4组:假手术组(Sham组)、缺血再灌注组(IR组)、H2S延迟预处理组(H2S组)和线粒体ATP敏感性钾通道(mitoKATP)阻滞剂5-HD+H2S组(5-HD组),每组8只。除假手术组,余3组通过结扎在体心脏冠状动脉前降支30min,松开复灌120min进行IR模型制备。再灌注末电镜下观察各组大鼠心肌细胞超微结构的变化,采用免疫印迹法检测各组心肌细胞中Bcl-2和Bax蛋白的表达。结果:4组间Bcl-2和Bax蛋白的表达,差异有统计学意义(F=31.937和11.681,P<0.001)。与IR组相比,H2S组Bcl-2蛋白上调和Bax蛋白下调(P均<0.05),5-HD组差异无统计学意义(P均>0.05)。结论:H2S延迟预处理具有心肌保护作用,其机制可能与调节细胞凋亡及激活mitoKATP有关。Aim：To observe the cytoprotection of hydrogen sulfide delayed preconditioning on myocardial ischemic reperfusion injury in rats and the possible mechanism.Methods：Thirty-two male SD rats were randomly divided into 4 groups：group sham,IR group（group IR）,hydrogen sulfide treatment group（group H2S）and 5-HD＋H2S group（group 5-HD）.IR model was made by ligation of the anterior descending coronaryartery for 30 min followed by 120 min reperfusion.We observed myocardial ultrastructure under electron microscope and detected myocardial Bcl-2 and Bax protein by western blotting.Results：The expressions of Bcl-2 and Bax protein among 4 groups were different,there were obvious differences（F=31.937 and 11.681,P0.001）.The expressions of Bcl-2 protein was higher and Bax protein was lower in group IR than in group H2S（P0.05）;there was no significant difference in group IR and in group 5-HD（P0.05）.Conclusion：Hydrogen sulfide protect myocardial function.Regulation of cell apoptosis and activating mitoKATP are the possible mechanisms.

关 键 词：硫化氢 缺血再灌注 凋亡 线粒体ATP敏感性钾通道 大鼠 

分 类 号：R542.2[医药卫生—心血管疾病]