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  

Effects of tanshinoneⅡA pretreatment on neuroprotectant and GFAP expression in rats of focal cerebral ischemia-reperfusion injury

作　　者：陈卫银[1] 孙承铭[2] 王会民[2] 朱观祥[2] 祝彼得[2] 马岱朝[2] 刘福友[1] 

机构地区：[1]成都中医药大学附属医院,成都610072 [2]成都中医药大学

出　　处：《山东医药》2011年第8期35-37,共3页Shandong Medical Journal

基　　金：四川省中医药管理局课题(2006-c-SZYJ-01);成都中医药大学校基金重点课题(2R2D200403)

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。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.

关 键 词：丹参酮ⅡA 胶质细胞酸性蛋白 星形胶质细胞 神经保护 

分 类 号：R743.31[医药卫生—神经病学与精神病学]