黄芪预处理对家兔心肌缺血再灌注后心肌线粒体结构及功能的影响  

Protective effect of Astragalus hoangtchy preconditioning on myocardial mitochondria in ischemia reperfusion injury in rabbits

作　　者：王小燕[1] 景桂霞[1] 

机构地区：[1]西安交通大学医学院第一附属医院麻醉科,陕西西安710061

出　　处：《西安交通大学学报（医学版）》2008年第3期329-332,共4页Journal of Xi’an Jiaotong University（Medical Sciences）

基　　金：陕西省科技攻关项目资助(No.2006K16-G14)

摘　　要：目的观察黄芪预处理对兔心肌缺血再灌注时心肌线粒体功能及结构的影响。方法将家兔32只随机分为假手术组(A组)、心肌缺血再灌注组(B组)、黄芪预处理组(C组)和5-羟葵酸加黄芪预处理组(D组),每组8只动物。观察线粒体Ca2+浓度、丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性及线粒体超微结构的改变。结果黄芪预处理组SOD活性明显高于心肌缺血再灌注组(P<0.05),而Ca2+浓度、MDA含量则低于心肌缺血再灌注组(P<0.05,P<0.01)。5-羟葵酸加黄芪预处理组与心肌缺血再灌注组各指标比较,差异无统计学意义。黄芪预处理组同心肌缺血再灌注组和5-羟葵酸加黄芪预处理组相比较,线粒体超微结构损伤明显减轻。结论黄芪可降低线粒体氧自由基水平、减轻线粒体钙超载,从而改善缺血再灌注心肌的线粒体结构及功能,发挥心肌保护作用,且其很可能通过线粒体ATP敏感性钾通道发挥作用。Objective To observe the protective effect of Astragalus hoangtchy preconditioning on myocardial ischemia reperfusion injury in rabbits and structural and functional changes of mitochondria so as to provide prevention evidence of Astragalus hoangtchy being taken into clinical treatment for myocardial ischemia reperfusion injury. Methods Thirty-two healthy male rabbits were divided randomly into four groups： sham-operation group （Group A）, ischemic reperfusion group （Group B）, astragalus hoangtchy preconditioning group （Group C） and 5-HD plus Astragalus hoangtchy preconditioning group （Group D）, with eight rabbits in each. All rabbits in the four groups were killed 2h after reperfusion. We examined Ca2＋ concentration, MDA content, and SOD activity of myocardial mitochondria and observed ultrastructural changes of myocardium under electron microscope. Results SOD activity of myocardial mitochondria in Group C was significantly higher than that in Group B （P〈0.05）. Ca2＋ concentration and MDA content in Group C were much lower those in Group B （P 〈 0. 05, P 〈0. 01）. No significant difference was found in indicators between Group B and Group D. Ultrastructural injuries of myocardial mitochondria in Group C were milder than those in Group D. Conclusion Astragalus hoangtchy preconditioning can alleviate Ca2＋ overload and increase SOD activity and decrease MDA content in myocardial mitochondria when ischcmia reperfusion occurs. The mechanism of protection can alleviate myocardial ischemia reperfusion injury, which may act depending on mitochondrial ATP-sensitive potassium channel.

关 键 词：黄芪 预处理 心肌 缺血再灌注损伤 线粒体 

分 类 号：R285[医药卫生—中药学]