丹参酮ⅡA预处理对局灶性脑缺血再灌注损伤大鼠神经保护作用及GFAP表达的影响

摘要

Objective To investigate the underlying mechanism of the neuronprotective effects of Tanshinone Ⅱ A 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 Ⅱ A pretreatment group, sham-operated group,and blank group. MCAO model was established by the method of Zea Longa. Rats in Tanshinone Ⅱ A pretreatment group received continuously treatmented with Tanshinone Ⅱ A 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 Ⅱ A pretreatment exhibit less pathological lesion than NS + MCAO group. Expression of GFAP in Tanshinone Ⅱ A pretreatment group was higher than that in NS + MCAO group ( P ＜ 0.05 ). Conclusion Tanshinone Ⅱ A pretreatment exhibits a neuroprotective effect against cerebral ischemic-reperfusion injury. The underlying mechanism may involve astrocyte activation.%目的 探讨丹参酮Ⅱ A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.