Neuroprotective effects of a mitochondrial K^+-ATP channel opener (diazoxide) are mediated by Bcl-2 expression upregulation  

作　　者：Majid Katebi Mansooreh Soleimani Mehdi Mehdizadeh 

机构地区：[1]Department of Anatomy,School of Medicine,Hormozgan University of Medical Sciences [2]Cellular and Molecular Research Center,Tehran University of Medical Sciences [3]Department of Anatomy,School of Medicine,Tehran University of Medical Sciences [4]Research Institute for Islamic & Complementary Medicine,Tehran University of Medical Sciences

出　　处：《Neural Regeneration Research》2011年第12期956-960,共5页中国神经再生研究（英文版）

摘　　要：Mitochondrial K＋-ATP （mito-KATP） channels play an important role in cellular function and survival following ischemic stress. The present results revealed that intervention with diazoxide, a mito-KATP channel opener, led to an increase in Bcl-2 expression in the cerebral cortex of rats subjected to cerebral ischemia reperfusion injury. In addition, the intervention also led to clear improvements in neuronal mitochondrial morphology and consciousness post-injury. Glibenclamide a mito-KATP channel blocker, exhibited the converse effects. Both diazoxide and glibenclamide exerted dose-dependent effects （in particular, at 18 mg/kg diazoxide and 25 mg/kg glibenclamide）. These findings suggest that diazoxide exerts a neuroprotective effect on cerebral ischemia reperfusion injury by opening mito-KATP channels and upregulating Bcl-2 expression.Mitochondrial K＋-ATP （mito-KATP） channels play an important role in cellular function and survival following ischemic stress. The present results revealed that intervention with diazoxide, a mito-KATP channel opener, led to an increase in Bcl-2 expression in the cerebral cortex of rats subjected to cerebral ischemia reperfusion injury. In addition, the intervention also led to clear improvements in neuronal mitochondrial morphology and consciousness post-injury. Glibenclamide a mito-KATP channel blocker, exhibited the converse effects. Both diazoxide and glibenclamide exerted dose-dependent effects （in particular, at 18 mg/kg diazoxide and 25 mg/kg glibenclamide）. These findings suggest that diazoxide exerts a neuroprotective effect on cerebral ischemia reperfusion injury by opening mito-KATP channels and upregulating Bcl-2 expression.

关 键 词：K-ATP channel BCL-2 cerebral ischemia reperfusion injury DIAZOXIDE 

分 类 号：R741[医药卫生—神经病学与精神病学]