Mitochondrial calcium uniporter opener spermine attenuates the cerebral protection of mitochondrial ATP-sensitive potassium channels through peroxidation in rats

OBJECTIVE: Animal models of transient ischemia suggest that mitochondrial ATP-sensitive potassium channels (mitoKATP) could constitute the main protectve effect of ischemia-reperfusion injury. While the mechanism of diazoxide is vague, the role of mitochondrial calcium uniporter (MCU) in the effect of diazoxide remain unknown. We aimed to determine the effect of mitochondrial calcium uniporter opener spermine on the protection of diazoxide against transient cerebral ischemia-reperfusion injury in rats.

MATERIALS AND METHODS: We chose adult male Wistar rats to constitute the transient middle cerebral artery occlusion (MCAO) model. Animals were randomly divided into five groups: the Sham group, the I/R group, the Dzx + I/R group, the Dzx + Sper +I/R group, and the Sper + I/R group. Rats were exposed to 24h reperfusion after 2h ischemia. All rats were given neurological performance tests after 24h reperfusion, then their brains were excised for infarct volume and biochemical evaluation and analysis.

RESULTS: The beneficial effects of diazoxide were significantly attenuated by treated with spermine through aggravating neurological deficits, infarct volume and oxidative stress (evidenced by increased malondialdehyde and nitric oxide, while decreased antioxidant enzymes [e.g., superoxide dismutase and glutathione peroxide]).

CONCLUSIONS: The present results suggested diazoxide-induced cerebral protection against transient cerebral ischemia-reperfusion is mediated by mitochondrial calcium uniporter.

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