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

作者：Katebi Majid; Soleimani Mansooreh; Mehdizadeh Mehdi^*

来源：Neural Regeneration Research, 2011, 6(12): 956-960.

DOI：10.3969/j.issn.1673-5374.2011.12.014

• K-ATP channel
• Bcl-2
• cerebral ischemia reperfusion injury
• diazoxide

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.

• 出版日期2011-4-25