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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 18mg/kg diazoxide and 25mg/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 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 The findings suggest that diazoxide exerts a neuroprotective effect on cerebral ischemia reperfusion injury by opening mito-KATP channels and upregulating Bcl-2 expression.