This paper investigates the damage mechanism of rat hippocampal neurons induced by the ischemia reperfusion and the intervention of the Edaravone. An ischemia reperfusion model is built by the middle cerebral artery occlusion (MACO)-reperfusion method. The reperfusion is performed 2 hours after the ischemia and persists for 22 hours (24 h since surgery). According to the Zea Longa's 5 level evaluation method, the neurobehavioral score of rats is graded; The rats' tissue pathological morphological changes are observed by the HE staining; the expressions of amyloid β (Aβ) and its precursor (APP) in the hippocampus of rats are detected with the immunohistochemistry, the image analysis and the Western Blot. It is shown that the model group rats show obvious symptoms of the nerve function defect; By contrast, the Edaravone of 6 and 10 mg/kg could improve model rats' symptoms of the nerve defect in varying degrees; And the difference is more significant in 10 mg/kg group (P<0.01). The HE staining shows that the depigmentation of the model group rat hippocampal neurons is obvious, and the two treatment groups could reduce this kind of morphology change; The immunohistochemistry and Western Blot analysis results suggest that both levels of Aβ and APP in the model group are significantly higher than those in the sham group (P<0.01), however, in different concentrations of Edaravone groups, their expression is significantly reduced (P<0.05). It is concluded that the ischemia reperfusion could cause neuron cells' damage by increasing Aβ and APP, and the Edaravone might suppress their toxic effects and protect the neuron cells by decreasing their expression.

cerebral ischemia reperfusion  /  β amyloid  /  amyloid precursor protein  /  Edaravone