【摘要】 目的探讨丹参酮ⅡA预处理对局灶性脑缺血的保护作用及其作用机制。方法将60只SD大鼠随机分为4组:生理盐水+大脑中动脉梗死组(NS+MCAO组)、丹参酮ⅡA预处理组、假手术组和空白组。采用ZeaLonga线栓法造大脑中动脉梗死模型,观察各组组织病理学改变,测定胶质细胞酸性蛋白(GFAP)的表达水平。结果丹参酮ⅡA预处理能减轻局灶性脑缺血模型大鼠的神经损伤,丹参酮ⅡA预处理组GFAP表达程度较NS+MCAO组高(P<0.05)。结论丹参酮ⅡA预处理能够促进缺血后星型胶质细胞活化增殖,减轻缺血性脑损伤。更多还原

【Abstract】 Objective To investigate the underlying mechanism of the neuronprotective effects of Tanshinone ⅡA against cerebral ischemic-reperfusion injury.Methods A total of 60 rats were randomly divided into 4 groups: normal saline and middle cerebral artery occlusion(NS+MCAO) group,Tanshinone ⅡA pretreatment group,sham-operated group,and blank group.MCAO model was established by the method of Zea Longa.Rats in Tanshinone ⅡA pretreatment group received continuously treatmented with Tanshinone ⅡA at 15 mg/(kg·d) for 3 days before MCAO.Pathological change was detected by HE stain.Expression of glial fibrillary acidic protein(GFAP) was detected by immunostaining.Results Tanshinone ⅡA pretreatment exhibit less pathological lesion than NS+MCAO group.Expression of GFAP in Tanshinone ⅡA pretreatment group was higher than that in NS+MCAO group(P<0.05).Conclusion Tanshinone ⅡA pretreatment exhibits a neuroprotective effect against cerebral ischemic-reperfusion injury.The underlying mechanism may involve astrocyte activation.更多还原