mitochondrial K-ATP channel opener, diazoxide, protects brain against ischemia-reperfusion injury in the rat

ABSTRACT

Even today there is no effective drug therapy to prevent neuronal loss after brain stroke. The objective of this research was to study effects of the mitochondrial K-ATP [MAK] channel regulators on neuronal cell population and neurological function after ischemia reperfusion in the rat. Rats were temporarily subjected to four vessels occlusion for 15 minutes followed by 24 hours reperfusion with or without MAK channel regulators. The normal cell count of neuronal population significantly increased in the K-ATP channel opener [diazoxide] treated ischemia-reperfusion group compared with the control group. Cell count and neurological function scores were dose dependent to MAK channel regulators in vivo. Our results showed that diazoxide treatment leads to better preservation of cortical neurons in rat