K_(ATP)通道开放剂对丘脑神经元缺血/再灌注损伤的影响  

Influence mitochondrial ATP-sensitive potassium channel opener on mitochondrial functions of simulated ischemia/reperfusion injury in cultured thalamus neuron

作　　者：张辉[1] 喻莉萍[2] 李强国[1] 李旭[1] 李林珍[1] 李明[1] 彭名勇[1] 姚飞虹[1] 

机构地区：[1]湘南学院化学与生命科学系药学教研室,湖南郴州423000 [2]湘南学院图书馆,湖南郴州423000

出　　处：《中国医院药学杂志》2009年第21期1814-1816,共3页Chinese Journal of Hospital Pharmacy

基　　金：湖南省教育厅科学研究项目优秀青年资助项目(编号:08B072);湘南学院科学研究项目资助项目(编号:08Z002)

摘　　要：目的:探讨线粒体ATP敏感性钾通道对大鼠丘脑神经元缺血/再灌注损伤的影响。方法:采用培养大鼠丘脑神经元缺血/再灌注损伤模型,观察二氮嗪预处理对丘脑神经元缺血/再灌注损伤后细胞线粒体活性和线粒体膜电位影响。结果:二氮嗪预处理大鼠后,对培养大鼠丘脑神经元缺血/再灌注损伤有影响,能减少丘脑神经元线粒体活性和线粒体膜电位的下降。结论:线粒体ATP敏感性钾通道开放剂能产生预处理丘脑神经元线粒体保护效应。OBJECTIVE To investigate the affection of mitochondrial ATP sensitive potassiom channel by ischemia/reperfusion injury in cultured thalamus neuron. METHODS In model of simulated ischemia/reperfusion injury, rats were pretreated with diazoxide. The activity of mitochondria and the mitochondrial membrane potential were observed. RESULTS Compared with the controls the activity of mitochondria and the mitoehondrial membrane potential were decreased in ischemia/reperfusion group. Administration of diazoxide increased the activity of mitochondria and mitochondrial membrane potential. CONCLUSION Preconditioning by diazoxide can protect the function of mitochondria against thalamus neuron ischemia/reperfusion injury.

关 键 词：线粒体 ATP敏感性钾通道 缺血/再灌注 膜电位 

分 类 号：R963[医药卫生—微生物与生化药学]