| Objective:To investigate the mechanism of cerebral ischemia-reperfusion injury in rats hippocampal neurons and the effect of Edaravone.Methods:Cerebral ischemiareperfusion model was prepared by middle cerebral artery occlusion(MCAO)-reperfusion method.Reperfusion was performed 2 hours after ischemia and persisted till 22 and 46hours(24 h,48 h after surgery).According to the Zea Longa’s 5 levels evaluation method,the neurobehavioral score of rats was graded; the rats’ tissue pathological morphological changes was showed by HE staining; Expression of Aβ,APP and AQP4 in hippocampus of rats was detected with immunohistochemistry and Western Blot.Results:It was shown that model group rats(cerebral ischemia-reperfusion 24 h and48 h) had high neurobehavioral scores and showed obvious symptoms of nerve function defect,the neurobehavioral scores of Edaravone in 10 mg/kg group rats were significantly lower than the model group rats’(P < 0.05); HE staining showed that the neurons’ structure had been destroyed,but both of Edaravone in 6 mg/kg and 10 mg/kg could improve this kind of morphology damage; Immunohistochemistry and Western Blot analysis results suggested that both levels of Aβ and APP in the model group(cerebral ischemia-reperfusion 24 h) rats were significantly higher than those in the sham group(P< 0.01),however,in different concentrations of Edaravone groups,their expression was significantly reduced(P < 0.05); Immunohistochemistry and image analysis results suggested that the integral optical density(IOD) of AQP4 in hippocampal area of model group rats(cerebral ischemia-reperfusion 48 h) was significantly higher than sham-operated control group rats’(P<0.05),and the IOD of AQP4 in hippocampal area of Edaravone in 6 mg/kg and 10 mg/kg group rats was significantly lower than model group rats’(P < 0.05).Conclusion:Cerebral ischemia-reperfusion could cause neuron cells’ damage by increasing Aβ,APP and AQP4,Edaravone could reduce their expression level and improve the nerve defect symptoms. |