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目的观察雌激素对绝经后雌性大鼠缺血性脑损伤的保护作用及一氧化氮合酶表达的影响。方法随机将12月龄雌性大鼠分为假手术组(A组)、对照组(B组)、雌激素处理组(C组)、雌激素+他莫西芬处理组(D组),采用线栓法制作大鼠大脑中动脉闭塞(MCAO)模型,观察缺血后24h脑梗死体积、神经功能缺损程度;采用免疫组织化学法观察脑组织中神经元型NOS(nNOS)及内皮型NOS(eNOS)的表达水平。结果雌激素处理组及雌激素+他莫西芬处理组均较对照组脑梗死体积小、神经功能缺损轻,但雌激素处理组较雌激素+他莫西芬处理组脑梗死体积小、神经功能缺损轻;雌激素处理组较对照组nNOS表达降低,eNOS表达增强。结论雌激素对绝经后雌性大鼠缺血性脑损伤具有明显的保护作用,时间窗为6h;雌激素受体拮抗剂他莫西芬可部分阻断雌激素的神经保护作用;雌激素增强eNOS及降低nNOS的表达水平是神经保护作用的可能机制。
Objective To observe the protective effect of estrogen on ischemic brain injury and the expression of nitric oxide synthase in postmenopausal female rats. Methods 12-month-old female rats were randomly divided into sham operation group (group A), control group (group B), estrogen treatment group (group C) and estrogen + tamoxifen treatment group (group D) The middle cerebral artery occlusion (MCAO) model was established by the method of thread occlusion. The cerebral infarction volume and the degree of neurological deficit were observed 24h after ischemia. The expression of neuronal NOS (nNOS) and endothelial NOS eNOS) expression levels. Results Compared with the control group, the estrogen-treated group and the estrogen + tamoxifen-treated group were smaller in size and had less neurological deficits. However, the estrogen-treated group was smaller than the estrogen + Dysfunction and light. The expression of nNOS and the expression of eNOS in estrogen-treated group were lower than those in control group. Conclusion Estrogen has a protective effect on ischemic brain injury in postmenopausal female rats with a time window of 6h. Estrogen receptor antagonist tamoxifen can partly block the neuroprotective effect of estrogen. Estrogen enhances eNOS And reduce the level of nNOS expression is a possible mechanism of neuroprotective effect.