17β-雌二醇对雌性去卵巢大鼠缺血性脑损伤的神经保护作用及机制  

Neuroprotection and mechanism of 17β-estradiol in ovariectomized female rats with cerebral ischemia

作　　者：宋先兵[1,2] 陈天平[1] 陈晓宇[1] 姚玉芹[2] 陈晓蓉[1] 

机构地区：[1]安徽医科大学组织胚胎学教研室,合肥230022 [2]安徽医学高等专科学校人体解剖学与组织胚胎学教研室,合肥230061

出　　处：《安徽医科大学学报》2010年第6期763-766,共4页Acta Universitatis Medicinalis Anhui

基　　金：安徽省教育厅自然科学研究项目(编号:KJ2010A183)

摘　　要：目的探讨17β-雌二醇对雌性去卵巢大鼠缺血性脑损伤的神经保护作用及其可能机制。方法♀SD大鼠60只随机分为17β-雌二醇处理组(A组)、假手术组(B组)和对照组(C组),采用线栓法制作大鼠大脑中动脉栓塞(MCAO)模型,缺血24h后观察脑梗死体积、神经功能缺损程度和雌激素受体α(ERα)的表达。结果缺血24h后,A组较C组脑梗死体积小、神经功能缺损程度轻,ERα表达明显增多。结论 17β-雌二醇对雌性去卵巢大鼠缺血性脑损伤具有明显的神经保护作用;ERα可能直接介导了17β-雌二醇的神经保护作用。Objective To study the neuroprotection and mechanism of 17β-estradiol（E2） in ovariectomized female rats with cerebral ischemia.Methods The female Sprague-Dawley rats were randomly divided into three groups： E2-treated group,sham group and control group.The models of cerebral ischemia were made by occlusion of middle cerebral artery used an intraluminal filament method.The infarct volume,the neurological deficit scores and the expression of estrogen receptor α（ERα） were evaluated after 24 hours focal cerebral ischemia.Results Compared with control group,the infarct volumes and neurological deficit scores were significantly decreased in E2-treated group,while the expression of ERα increased significantly.Conclusion E2 may play a protective role on cerebral ischemia in ovariectomized rats and the ERα may directly mediate neuroprotection.

关 键 词：脑缺血 雌激素受体Α 卵巢切除术 

分 类 号：R743.3[医药卫生—神经病学与精神病学] R977.1[医药卫生—临床医学]