线粒体K_(ATP)通道开放对培养成年大鼠心肌细胞PKC epsilon转位激活的影响  

Effect of mitochondrial ATP sensitive potassium channels opening on translocation of protein kinase C epsilon in cultured adult rat ventricular myocytes

作　　者：李洪[1] 肖颖彬[2] 黄河[1] 杨天德[1] 

机构地区：[1]第三军医大学新桥医院麻醉科,重庆400037 [2]第三军医大学新桥医院心血管外科,重庆400037

出　　处：《中国病理生理杂志》2006年第3期439-442,共4页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.30200089)

摘　　要：目的:探讨MitoKATP通道特异性开放剂二氮嗪(DZ)预处理对PKCε的转位激活作用及其与活性氧生成的关系。方法:采用免疫荧光和Westernblotting等技术检测培养成年大鼠心室肌细胞PKCε的表达。结果:①MitoKATP通道特异性开放剂DZ预处理能引起PKCε向心肌细胞肌丝样结构转位;②活性氧清除剂2-巯基丙酰氨基乙酸(MPG)能抑制DZ预处理引起的PKCε转位;③PKC特性抑制剂氯化白屈菜赤碱(CH)能完全消除DZ预处理引起的PKCε转位。结论:MitoKATP通道开放能够激活PKCε向肌丝样结构转位。MitoKATP通道开放过程中生成的ROS是引起PKCε转位激活的重要原因。AIM： To investigate the effects of mitochondrial ATP sensitive potassium （MitoKATP） channel opening on translocation of protein kinase C epsilon （PKCε） and the relationship between the translocation of PKCε and the production of reactive oxygen species. METHODS： The expression of PKCε in cultured adult rat ventricular myocytes was investigated with immunofluorescence and Western blotting techniques. RESULTS： （ 1 ） Diazoxide, a selective MitoKATP channel opener, caused a significant translocation to myofibrillar- like structures in cultured adult rat ventricular myocytes. （2） The N - 2 - mercaptopropionylglycine （MPG）, a free radical scavenger, partly inhibited the translocation of PKCε caused by diazoxide. （3） Chelerythrine, a selective protein kinase C （PKC） inhibitor, completely blocked the translocation of PKCε caused by diazoxide. CONCLUSION： Opening of MitoKATP channel might activate PKCε and make it translocation to myofibrillar- like structures. PKCε activation occurs downstream of MitoKATP channel, and might be caused by production of reactive oxygen species after opening of MitoKATP channel.

关 键 词：线粒体 钾通道 心肌细胞 蛋白激酶C 

分 类 号：R363[医药卫生—病理学]