• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Opening of mitochondrial K(ATP) channel occurs downstream of PKC-epsilon activation in the mechanism of preconditioning.
【24h】

Opening of mitochondrial K(ATP) channel occurs downstream of PKC-epsilon activation in the mechanism of preconditioning.

机译：线粒体K（ATP）通道的开放发生在预处理机制中PKC-ε激活的下游。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

We examined whether the mitochondrial ATP-sensitive K channel (K(ATP)) is an effector downstream of protein kinase C-epsilon (PKC-epsilon) in the mechanism of preconditioning (PC) in isolated rabbit hearts. PC with two cycles of 5-min ischemia/5-min reperfusion before 30-min global ischemia reduced infarction from 50.3 +/- 6.8% of the left ventricle to 20.3 +/- 3.7%. PC significantly increased PKC-epsilon protein in the particulate fraction from 51 +/- 4% of the total to 60 +/- 4%, whereas no translocation was observed for PKC-delta and PKC-alpha. In mitochondria separated from the other particulate fractions, PC increased the PKC-epsilon level by 50%. Infusion of 5-hydroxydecanoate (5-HD), a mitochondrial K(ATP) blocker, after PC abolished the cardioprotection of PC, whereas PKC-epsilon translocation by PC was not interfered with 5-HD. Diazoxide, a mitochondrial K(ATP) opener, infused 10 min before ischemia limited infarct size to 5.2 +/- 1.4%, but this agent neither translocated PKC-epsilon by itselfnor accelerated PKC-epsilon translocation after ischemia. Together with the results of earlier studies showing mitochondrial K(ATP) opening by PKC, the present results suggest that mitochondrial K(ATP)-mediated cardioprotection occurs subsequent to PKC-epsilon activation by PC.
机译：我们检查了线粒体ATP敏感性K通道（K（ATP））是否在孤立的兔心脏预适应（PC）机制中是蛋白激酶C-ε（PKC-epsilon）的下游效应子。在进行30分钟的整体缺血之前，PC具有两个5分钟的局部缺血/ 5分钟的再灌注周期，将梗塞从左心室的50.3 +/- 6.8％降低到20.3 +/- 3.7％。 PC显着增加了颗粒级分中的PKC-ε蛋白，从占总数的51 +/- 4％增加到60 +/- 4％，而PKC-δ和PKC-α没有观察到易位。在线粒体与其他微粒部分分离的过程中，PC将PKC-ε水平提高了50％。 PC取消线粒体K（ATP）阻滞剂5-羟基癸酸酯（5-HD）时，取消了PC的心脏保护作用，而PC进行的PKC-ε易位并未干扰5-HD。二氮嗪是一种线粒体K（ATP）开启剂，在缺血前10分钟注入，将梗死面积限制为5.2 +/- 1.4％，但该药既不自身转运PKC-ε，也不在缺血后加速PKC-ε的转运。连同较早的研究结果表明线粒体K（ATP）被PKC打开，目前的结果表明，线粒体K（ATP）介导的心脏保护作用发生在PC激活PKC-ε之后。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号