大鼠全脑缺血再灌注后海马CA1区Bax蛋白表达与EGb761干预

Altered Expression of Bax in Hippocampus after Global Ischemia-Reperfusion and Protective Effect of EGb 761

目的观察大鼠全脑缺血再灌注后海马CA1区Bax蛋白的表达及超微结构的改变 ,并探讨EGb 76 1对脑缺血损伤的保护机制。方法将四血管阻塞法略作改动制成弥漫性全脑缺血 2 0min ,再灌注 2 4h、4 8h和 72h模型 ,实验动物随机分为三组 :假手术组 (SAM组 ) ,缺血再灌注组 (IR组 ) ,EGb 76 1治疗组 (EGb组 )。其中SAM组除不阻断椎动脉和颈总动脉外 ,余操作同实验组。采用SP法检测海马CA1区Bax蛋白表达 ,并应用透射电镜对该区超微结构进行观察。结果①Bax蛋白表达于再灌注 2 4h阳性信号最强 ,之后下降。②超微结构病理改变以 4 8h显著 ,2 4h病变不明显 ,72h神经细胞丢失严重。③治疗组Bax阳性信号较对应时间点的对照组明显减弱 ,超微病理改变也较轻。结论Bax蛋白在海马缺血后神经元迟发性死亡中起着重要作用 ,EGb 76

Objective To observe the altered expression of Bax protein and ultrastucture in CA1 region of hippocampus after global ischemia-reperfusion in rats,and to investigate the protective effect of Ginkgo biloba extract(EGb 761).Methods An global cerebral ischemia-reperfusion model of SD rats was established in Pulsinelli way.Healthy SD rats was divided into three groups at random:①Sham operated group(SAM),which is surgically exposed both cervicalarteries only.②Ischemia-reperfusion group(IR):global cerebral ischemia for 20min and reperfusion for 24h,48h and 72h respectively.③EGb 761-treated group(EGb):pretreated (7 days) with oral administration of EGb 761(100mg/kg·d -1 ).Immunohistochemistry staining(SP method) was used to detect Bax protein and TEM to morphologically observe the ultrastructure of injured neurons in CA1 region.Results A significant increase in Bax-positive expression was detected after reperfusion 24h,with much lower value at 72h after ischemia than SAM group.While Bax-positive expression in EGb group was obviously lower than that in IR group.In addition,ultrastructure of injured neurons in EGb group was markedly improved in comparison with IR group.Conclusion Bax protein played a very important role in the delayed neuronal death(DND) after global cerebral ischemia in hippocampus,and EGb 761 has highly protective effects against it, whose protective mechanism might be related to reducing the expression of Bax protein.