克罗卡林后处理对大鼠心肌缺血再灌注损伤的保护作用  

Effects of Cromakalim Induced Postconditioning on Ischemia Reperfusion Injury in Rats

作　　者：王国贤[1] 魏慧芳[1] 

机构地区：[1]辽宁医学院药理教研室,辽宁锦州121001

出　　处：《中华高血压杂志》2010年第7期677-680,共4页Chinese Journal of Hypertension

摘　　要：目的探讨克罗卡林后处理对大鼠心肌缺血再灌注损伤的保护作用及机制。方法采用左冠状动脉前降支结扎30min再灌120min建立大鼠心肌缺血再灌注模型。SD大鼠随机分为5组:假手术组,缺血再灌注组,缺血后处理组,克罗卡林后处理组,克罗卡林后处理+线粒体ATP敏感性钾通道阻断剂5-HD组,每组8只。观察心肌病理结构改变,肌酸激酶活性、超氧化物歧化酶(SOD)活性、丙二醛含量、三磷酸腺苷(ATP)含量变化和凋亡抑制蛋白Bcl-2、凋亡蛋白Bax表达的变化。结果克罗卡林后处理能减轻心肌损伤程度,使SOD活性增高,丙二醛含量降低,ATP含量增高,Bcl-2蛋白表达增加,Bax蛋白表达减少。加入线粒体ATP敏感性钾通道阻断剂5-HD后以上保护作用被阻断。结论克罗卡林后处理可减少缺血再灌注心肌损伤,增强心肌抗氧化能力,减少细胞凋亡,这种保护作用与激活线粒体ATP敏感性钾通道密切相关。Objective To observe the effects and mechanism of cromakalim (CR) induced postconditioning on myocardial ischemia reperfusion (IR) injury in rats. Methods A model of IR was obtained by ligating left anterior descending coronary artery for 30 minutes and followed by 120 minutes reperfusion. SD rats were randomly divided into five groups(n=8):sham operated group,IR group,postconditioning group (PostC),cromakalim induced postconditioning group (CRPC) and CRPC+5-HD(5-hydroxydecanoate,a mitochondrial ATP-sensitive potassium channel inhibitor) group. HE staining,contents of malondialdehyde (MDA) and adenosine tri-phosphate (ATP),activity of creatine kinase (CK) and superoxide dismutase (SOD),and expression of Bcl-2 and Bax were detected. Results In the CRPC group,activities of SOD were higher,contents of MDA were lower as compared to control group,contents of ATP were higher,Bcl-2 was higher,and Bax were lower. 5-HD abolished the protective effects induced by cromakalim. Conclusion CRPC could protect IR,enhance myocardial antioxygen capability,and inhibit apoptosis. The myocardial protective mechanism maybe related to mitochondrial ATP sensitive potassium channel.

关 键 词：克罗卡林 缺血后处理 凋亡 线粒体ATP敏感性钾通道 

分 类 号：R542.2[医药卫生—心血管疾病]