| Objective: To assess the neuroprotective efficacy of 2 , 4-dinitrophenol in the process of ischemia tolerance induced by global cerebral ischemia preconditioning (IP) in the adult rats.Materials and methods: The modified four-vessel occlusion rat model was applied in this experiment, 24 healthy Sprague-Dawley (SD) rats were divided randomly into 4 groups: Group A : sham operation. Group B (cerebral ischemia for 9 mins only). Group C :(IP for 3 minsand reperfusion for 72 hours--ischemia for 9 mins). Group D:( IP for 3mins and reperfusion for 72 hours--ischemia for 9 mins and thentreated with 2,4-dinitrophenol within one hour).All rats were decapitated 7 days later and the brain tissue were removed for histological examination.The histopathological and ultrastructural changes of cerebral hippocampus CA1 subarea were examined by HE staining, while the expressions of NGF-b and the mitochondrial release of cytochrome C were studied by immunohistochemistry. The experiment results were analyzed by statistical software and some drawings were made accordingly.Results: HE-stained thin brain slices showed: there was mass cell death in the ischemia-reperfusion group B, while no significant histological changes could be observed in sham operation group. And in group C and D, partly cell death demonstrated the neuroprotective effects of ischemia-preconditioning and 2,4-dinitrophenol. The expression of NGF-b and mitochondrial release of cytochrome C in immunohistological examination coincided with the result in HE staining. That was group C and D showed upregulation of NGF-b expression while less cytochrome C released from mitochondria.Conclusions : (1)The ischemia tolerance induced by cerebral ischemia preconditioning showed significant neuroprotective efficacy. (2) The mitochondrial uncoupler 2,4-dinitrophenol could prevent cell death effectively when delivered to rats at a mild dosage. |
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