摘要
目的:观察线粒体ATP敏感性钾通道(mitoKATP)及活性氧(ROS)在缺氧脑保护中的作用及其相互关 系。方法:采用脑片灌流及电生理学技术,细胞外记录海马CAl区的群体锋电位(PS)和缺氧去极化电位(HD)。结 果:用mitoKATP开放剂diazoxide(300 μmol／L)预处理海马脑片,可延长HD的潜伏期及缺氧后PS消失的时间,提高复 氧后PS的恢复率。该作用可被mitoKATP阻断剂5-hydroxydecanoic acid(200 μmol／L)所阻断。以ROS清除剂N-2- mercaptopropionyl glycine(MPG)(500μmol／L)预处理海马脑片,可减弱diazoxide的作用。单独使用MPG对PS及HD 无明显影响。结论:ROS介导了mitoKATP开放剂对缺氧脑的保护作用。
AIM： To examine whether reactive oxygen species （ROS） is involved in the neuroprotection by mitochondrial ATP- sensitive potassium channel （mitoKATP） in rat hippocampal slices during hypoxia. METHODS： The technique of electrophysiology was used, and the latency to hypoxic depolarization （HD） and the amplitude of population spike （PS） in the stratum pyramidale of the CA1 region were measured. RESULTS： Pretreatment of the slices with diazoxide （DIA, a mitoKATP opener, at concentration of 300 μmol/L）, prolonged the latency to HD, delayed the onset of PS disappearance and improved the recovery of PS after reoxygenation, The effects induced by DIA were attenuated by 5 - hydroxydecanoic acid （a mitoKATP blocker, at concentration of 200μmol/L）. Pretreatment with N - 2 - mercaptopropionyl glycine （MPG, a ROS scavenger, at concentration of 500μmol/L）, also abrogated the effects induced by DIA, while treatment of MPG alone had no effect on PS and HD. CONCLUSION： ROS participates in neuroprotection offered by mitoKATP opener during hypoxia.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2005年第10期2018-2021,共4页
Chinese Journal of Pathophysiology
基金
浙江省教育厅科研项目(No.20030306)
浙江大学医学院中青年科研启动基金资助项目
关键词
线粒体
钾通道
缺氧
脑
活性氧
Mitochondria
Potassium channels
Hypoxia, brain
Reactive oxygen species
