大鼠心肌缺血再灌注损伤对Kir6.1和Kir6.2通道亚基表达的研究  

A Research about Regulation of Kir6.1 and Kir6.2 Channel Subunits: Expression after Myocardial Ischemia-Reperfusion Injury in Rat Heart.

作　　者：陈灼焰 [1] 吴黎明  林庆芳 [1] 

机构地区：[1]350009,福州市,福州市第一医院,心内科 [2]350001,福州市,福建省医科大学附属协和医院,冠心病研究所

出　　处：《中国分子心脏病学杂志》2005年第5期721-724,共4页Molecular Cardiology of China

摘　　要：目的探讨缺血再灌注损伤大鼠心肌中,Kir6.1与Kir6.2通道亚基基因及蛋白水平表达的改变。方法雄性SD大鼠14只,体重250～300g,随机分为:假手术组、缺血再灌注损伤(IRI)组,每组各7只。RT—PCR方法检测。Kir6.1、Kir6.2mRNA的表达;WesternBlot方法检测细胞膜Kir6.1与Kir6.2蛋白的表达;同时应用放免法检测血浆AngⅡ与缺血区、非缺血区的心肌AngⅡ含量。结果(1)IRI引发缺血区及非缺血区Kir6.1mRNA水平明显升高,而Kir6.2mRNA水平没有明显改变;(2)IRI引发缺血区及非缺血区心肌细胞膜Kir6.1蛋白水平明显升高,而Kir6.2蛋白水平没有明显改变。结论IRI导致心肌KATP通道亚基构成发生了改变,可能与局部RAS的激活有一定的关系。Objective In this study, we investigated the changes in the gene and protein expression of Kir6.1 and Kir6.2 channel subunits after myocardial ischemia-reperfusion injury （IRI） in the rat heart. Methods Experiments were performed on 14 male SD rats （weighed 250-300 g） which were randomly divided into sham operation group and IRI group. Each group consisted of.7 rats. The expression levels of Kir6.1 ,Kir6.2 mRNA were determined with RT-PCR, and the expression levels of sarcolemmal Kir6. 1, Kir6.2 protein were examined by Western Blot. Plasma levels of Ang Ⅱ and cardiac tissue levels of Ang Ⅱ] in the ischemie and non-ischemie regions were measured by means of radio-immunoassay. Results （ 1 ） IRI caused a significant increase in Kir6.1 mRNA in the isehemie and no-isehemie regions as eompared with sham operation group. But there are no significant changes of Kir6.2 mRNA; （2） In parallel with the changes in mRNA level, sarcolemmal Kir6.1 protein was significantly augmented in the ischemie and no-isehemie regions after IRI. And there are no significant changes of sarcolemmal Kir6.2 protein. Conclusion Perhaps the activation of local renin-angiotensin system may play a role in induction of cardiac KATP channel subunit expression under IRI.

关 键 词：缺血再灌注损伤 Kir6.1 KIR6.2 血管紧张素Ⅱ 

分 类 号：R541[医药卫生—心血管疾病]