The Impact Of Aescinate In COX-2 In Focal Cerebral Ischemia Reperfusion Injury

Objective To study the effect of Aescinate on the expression of Cyclooxygenase-2(COX-2) in rats with cerebral ischemia reperfusion injury. Explore the protection and possible mechanisms of Aescinate on cerebral ischemia reperfusion injury in rats.Methods 132 healthy male Sprague-Dawley rats were randomly divided into the sham operated group, the model group and the treatment group. The latter two groups were separately divided into the reperfusion 6h (24h,48h,3d,5d)group Again. There were 12 rats in each group. Rats were selected to establish focal cerebral ischemia reperfusion model by middle cerebral artery thread embolism method. Sham-operated group only separation common carotid artery and external carotid artery. During surgery rats were heated with incandescent light to maintain a constant body temperature (rectal temperature 37℃). After wake rats appear embolization of the ipsilateral Horner syndrome and the contralateral limb movement disorder mean the model was successful. It was showed of the left forelimb can not be extended, walking to the left of the dumping or according to counter-clockwise circular. Otherwise rats were excluded. The treatment group instantly intraperitoneal injection Aescinate 5mg/kg/d After successful model, the rest of the group intraperitoneal injection equal saline. At the different time Rats in each group were respectively conducted the neurological deficit scores. The COX-2 expression in brain tissue was detected by immunohistochemistry method, the infarct sizes were measured with TTC staining and the pathological changes was observed by HE staining.Results The expression of COX-2 in focal cerebral ischemia reperfusion injury was located in infarction edge, frontal, parietal, cingulate cortex and the hippocampus, while in the center area of infarction, contralateral lesion, and sham-operated group brain tissue expression COX-2 less. After focal cerebral ischemia reperfusion 6 h, COX-2 expression began to increase,48h reached the peak, and then began to decrease, it was fell to a lower level at 5d, but still higher than normal. Aescinate could significantly reduce the COX-2 expression in cerebral tissue, when compared with the different time model group(P＜0.05). Aescinate could improve neurological symptoms, reduce infarct volume, indicating that it can reduce cerebral ischemia reperfusion injury, compared with ischemia reperfusion model group was statistically significant (P<0.05).Conclusion Aescinate could improve the cerebral ischemia reperfusion injury induced neurobehavioral disorder, reduce infarct size, lighten brain tissue degeneration, necrosis and other pathological damage. By reducing the expression of COX-2, Aescinate play a protective role on focal cerebral ischemia reperfusion injury.