Majid Katebi1, Mansooreh Soleimani2, 3, Mehdi Mehdizadeh2, 3, 4

1Department of Anatomy, School of Medicine, Hormozgan University of Medical Sciences, Bandar Abbas, Iran
2Cellular and Molecular Research Center, Tehran University of Medical Sciences, Tehran, Iran
3Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran 
4Research Institute for Islamic & Complementary Medicine, Tehran University of Medical Sciences, Tehran, Iran

Abstract
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.
Key Words: K-ATP channel; Bcl-2; cerebral ischemia reperfusion injury; diazoxide

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