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盐酸右美托咪定预处理对缺血-再灌注损伤大鼠心肌Bax和Bcl-2表达的影响
引用本文:陈盼,赵明,蒋鹏,王胜军,谷腾飞.盐酸右美托咪定预处理对缺血-再灌注损伤大鼠心肌Bax和Bcl-2表达的影响[J].重庆医学,2012,41(16):1604-1606,1673.
作者姓名:陈盼  赵明  蒋鹏  王胜军  谷腾飞
作者单位:江苏省镇江市江苏大学附属医院麻醉科,212000
基金项目:江苏省镇江市科技支撑-社会发展项目,江苏大学临床医学科技发展基金
摘    要:目的研究盐酸右美托咪定对大鼠心肌缺血-再灌注损伤时心肌凋亡相关基因Bax和Bcl-2表达的影响。方法将21只健康SD大鼠随机分为3组:假手术组(sham组,n=7)、缺血-再灌注组(I/R组,n=7)、缺血-再灌注+盐酸右美托咪定组(DEX组,n=7)。采用结扎左冠状动脉前降支的方法制备在体大鼠心肌缺血-再灌注损伤模型。采用RT-PCR、免疫组化方法检测Bcl-2和Bax mRNA、蛋白的表达,TUNEL法检测凋亡细胞TTC染色测定心肌梗死面积。结果与sham组比较,I/R组Bcl-2和Bax mRNA和蛋白表达增加(P<0.05);与I/R组比较,DEX组Bcl-2mRNA和蛋白表达升高(P<0.05),Bax mRNA和蛋白表达下降(P<0.05),凋亡细胞明显减少(P<0.01),心肌梗死面积减小(P<0.05)。结论盐酸右美托咪定预处理可上调心肌缺血-再灌注损伤大鼠心肌Bcl-2mRNA和蛋白表达,下调Bax mRNA和蛋白表达,表明盐酸右美托咪定在心肌缺血-再灌注损伤中有抗凋亡的作用。

关 键 词:心肌缺血  心肌再灌注损伤  细胞凋亡  基因  bcl-2  右美托咪定

Effects of dexmedetomidine on myocardial expression of Bax and Bcl-2 in rat myocardial ischemia/reperfusion injury
Chen Pan , Zhao Ming , Jiang Peng , Wang Shengjun , Gu Tengfei.Effects of dexmedetomidine on myocardial expression of Bax and Bcl-2 in rat myocardial ischemia/reperfusion injury[J].Chongqing Medical Journal,2012,41(16):1604-1606,1673.
Authors:Chen Pan  Zhao Ming  Jiang Peng  Wang Shengjun  Gu Tengfei
Institution:(Department of Anesthsiology,Affiliated Hospital of Jiangsu University,Zhenjiang,Jiangsu212000,China)
Abstract:Objective To investigate the effect of dexmedetomidine on the expression of Bcl-2 and apoptosis related protein Bax in rat myocardium apoptosis during ischemia reperfusion.Methods 21 healthy male Sprague-Dawley rats were randomly divided into 3 groups: sham group,I /R group(I/R group) and IR+dexmedetomidine group(DEX group).Ligation of left anterior descending coronary artery was performed for establishing the rat myocardial ischemia/reperfusion injury mode in vivo.Real-time and immunohistochemistry were used to analyze the expression of Bcl-2 and Bax at mRNA and protein leves,TUNEL was used to analyze apoptoic index and TTC staining was adopted to investigate the infract size.Results Compared with the sham group,the expression of Bcl-2 at mRNA and protein level were increased in the I/R group(P<0.05),the expression of Bax at mRNA and protein level was significantly increased in the I/R group(P<0.05).Compared with the I/R group,the expression of Bcl-2 at mRNA and protein level was heightenend(P<0.05) in the DEX group,Bax at mRNA and protein level was decreased in the DEX group(P<0.01).The infract size and apoptotic index were reduced compared with the IR group.Conclusion Dexmedetomidine can inhibit the apoptosis of myocardium by up-regulating the expression of Bcl-2 and down-regulating the expression of Bax at mRNA and protein level,which may be part of the molecular mechanism of dexmedetomidine on myocardial preservation.
Keywords:myocardial ischemia  myocardial reperfusion injury  apoptosis  gene  bcl-2  dexmedetomidine
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