人重组硫氧还蛋白对大鼠心肌缺血再灌注梗塞范围和心肌凋亡的影响  

Effects of human thioredoxin on infarction size and apoptosis induced by ischemiareperfusion in rats

作　　者：武小薇[1] 张一娜[1] 滕宗艳[1] 姜礼红[1] 范鹰[1] 胡萍萍[1] 

机构地区：[1]哈尔滨医科大学附属二院老年病科,黑龙江哈尔滨150086

出　　处：《心血管康复医学杂志》2009年第1期26-29,49,共5页Chinese Journal of Cardiovascular Rehabilitation Medicine

基　　金：哈尔滨市科委基金(编号:2003AFQXJ039)

摘　　要：目的:探讨人重组人硫氧还蛋白对大鼠心肌缺血再灌注后心肌梗塞范围和心肌细胞凋亡的影响。方法:成年Wister大鼠被随机分为3组;Ⅰ组:假手术组(8只),Ⅱ组:缺血再灌注组(7只),Ⅲ组:人重组硫氧还蛋白保护组(6只)。Ⅱ、Ⅲ组分别在结扎左室前降支30min后再灌注120min,Ⅲ组再灌注后立即静脉注人重组硫氧还蛋白。观察再灌注后心肌梗塞范围和心肌细胞凋亡以及凋亡相关基因的表达。结果:人重组硫氧还蛋白显著降低了再灌注后心肌梗塞范围和心肌细胞凋亡数量(P均<0.01),并上调凋亡相关基因bcl-2的表达(P<0.05)。结论:人重组硫氧还蛋白对心肌缺血再灌注具有保护作用,其抑制凋亡的作用可能是通过上调bcl-2基因表达来发挥的。Objective： This study was conducted to explore the role of human thioredoxin on myocardial ischemia/reperfusion injury and its potential mechanisms. Methods： The Wister rats randomly divided into three groups： sham group （8 cases）, ischemia/reperfusion （I/R） group （Wister rats were suffered to 30 rain of myocardial ischemia followed by 120 min of reperfusion, 8 cases）, and thioredoxin group （purified human thioredoxin was injected into adult Wister rats treated as same as group I/R, 5 cases）. At the end of study, the infarct size was determined by tetrazolium chloride staining, cardiomyocyte apoptosis was detected by TdT mediate dUTP nick end labeling （TUNEL） assay, and the protein expression of Bcl--2 and Bax in myocardium were assayed by immunochemistry. Results： Human thioredoxin reduced myocardial ischemia/reperfusion injury as evidenced by significant decrease of myocardial infarct size （P〈0.01） and notable reduction of cardiomyocyte apoptosis （P〈0.01）. Furthermore, human thioredoxin markedly increased protein expression of Bcl-2 （P〈0.05）. Conclusion： These results strongly suggest that human thioredoxin has effects on anti-myocardial ischemia/reperfusion and its anti--apoptotic role is mediated, at least in part, by up-regulation of bcl-2.

关 键 词：硫氧还蛋白 再灌注 心肌梗塞 细胞凋亡 

分 类 号：R542.2[医药卫生—心血管疾病] R285.5[医药卫生—内科学]