缺血后处理减轻心肌线粒体损伤对缝隙连接蛋白43的影响  

Effect of ischemic postconditioning on injury and connexin Cx43 of mitochondria

作　　者：何燕[1] 曾志羽[1] 钟国强[1] 李薇[1] 李金轶[1] 李伟科[1] 

机构地区：[1]广西医科大学第一附属医院老年心内科,南宁530021

出　　处：《中华老年心脑血管病杂志》2011年第8期742-745,共4页Chinese Journal of Geriatric Heart,Brain and Vessel Diseases

基　　金：国家自然科学基金(309601 31);广西医疗卫生重点科研课题(200848)

摘　　要：目的观察缺血后处理对线粒体缝隙连接蛋白43(Cx43)的影响以及心肌保护的可能机制。方法健康新西兰大白兔64只.建立心肌缺血再灌注模型,随机分为4组,假手术组、缺血再灌注组、缺血预处理组、缺血后处理组,每组16只。检测各组心肌梗死面积,透射电镜观察心肌细胞的超微结构,荧光法检测线粒体膜电位,比色法检测线粒体Ca^(2+)和丙二醛浓度及超氧化物歧化酶(SOD)活性,Western blot法检测Cx43含量。结果与缺血再灌注组比较,缺血后处理组和缺血预处理组兔心肌梗死面积明显减少,心肌线粒体形态结构改变明显减轻,跨膜电位、SOD活性、线粒体Cx43明显升高,Ca^(2+)、丙二醛浓度明显降低(P<0.05,P<0.01)。与假手术组比较,缺血再灌注组兔线粒体Cx43明显下调(P<0.05)。结论缺血后处理保护心肌及线粒体可能与提高线粒体跨膜电位、降低线粒体氧自由基水平和减轻线粒体Ca^(2-)超载有关,其机制可能与提高线粒体Cx43表达有关。Objective To observe the impact of ischemic posteonditioning on mitochondrial connexin 43（Cx43） and the possible mechanisms of myocardial protection. Methods Sixty-four rabbits were randomly divided into four groups with sixteen rabbits each： sham operation group,ischemia/reperfusion group, ischemic preconditioning group and isehemic postconditioning group. All rabbits in the four groups were sacrificed 4 h after reperfusion. Myocardial infarct size and ultrastructural changes of mitochondria were observed, while membrane potential, Ca2＋ concentration, MDA content and SOD activity of myocardial mitochondria were examined at the end of the experiment. The content of the mitochondria Cx43 was detected with Western Blot. Results Compared with ischemia/reperfusion group,myocardial infarct size was significantly reduced （P 〈 0.01） and the damage of mitochondrial ultrastructure was lighter （P 〈 0. 05）, Ca2＋ concentration and MDA content were much lower,while membrane potential,SOD activity and mitochondria Cx43 expression were significantly higher （P 〈 0.05） in ischemic preconditioning group and ischemic postconditioning group （P 〈 0.05）. Compared with sham group,the mitochondria Cx43 expression in ischemia/reperfusion group was distinctly decreased. Conclusion Ischemic postconditioning can protect mitochondrial ultrastructure by increasing mitochondrial membrane potential and SOD activity,and also by alleviating Ca2＋ overload and decreasing MDA content in myocardial mitochon dria. The mechanism may be related to increasing expression of mitochondria Cx43.

关 键 词：心肌梗死 再灌注损伤 线粒体 心脏 连接蛋白类 缺血预处理 心肌 膜电位 丙二醛 超氧化物歧化酶 

分 类 号：R541[医药卫生—心血管疾病]