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

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Western blotting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。

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

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.