远端创伤预处理对心肌内向整流钾通道Kir6．2表达的影响  

Expression of Kir6. 2 in Rat Myocardial Cells after Remote Preconditioning of Trauma

作　　者：徐林[1] 张登文[1] 张传汉[1] 刘卫 田玉科[1] 王学仁[1] 

机构地区：[1]华中科技大学同济医学院附属同济医院麻醉科,武汉市430030 [2]济南军区第88医院药剂科,山东省泰安市271000

出　　处：《医学分子生物学杂志》2013年第3期136-138,共3页Journal of Medical Molecular Biology

基　　金：教育部博士点基金新教师项目（No.20070487131）,湖北省卫生厅青年科技人才基金（No.QJX2008-1）

摘　　要：目的观察远端创伤预处理后心肌细胞内向整流K^＋通道Kit6．2在不同时点的表达变化。方法SD大鼠腹部做一长2cm的横切口后，分别于15min、4h、24h时间点取大鼠左心室心肌，检测其内向整流K^＋通道Kit6．2的蛋白表达的变化。结果远端创伤预处理后，随时间的推移心肌细胞内向整流K^＋通道Kit6．2的蛋白表达量逐渐增加。结论远端创伤预处理可以上调心肌细胞内向整流K^＋通道Kit6．2的表达，这可能参与了远端创伤预处理对心肌缺血再灌注损伤的保护作用。Objective To investigate the expression of Kit6.2 in myocardial cells after remote preconditioning of trauma （RPCT） at different time points. Methods A transverse incision 2 cm in length was made in a SD rat. Left ventricular myocardial tissue was harvested at 15 rain, 4 h and 24 h after operation. The expression of Kit6. 2 was measured. Results After RPCT, the protein expression level of Kit6.2 in myocardial cells was increased with time. Conclusion RPCT may increase the expression of inward rectifier K＋ channel Kir6. 2 in myocardial cells, suggesting that Kit6.2 may participate in the protection of RPCT in cardiac reperfusion injury （CRI） .

关 键 词：KATP 心肌保护 缺血再灌注损伤 

分 类 号：R349.92[医药卫生—基础医学]