神经保护和雌激素

Neuroprotection and estrogen

目的:探讨雌激素的神经保护作用机制,并观察其在临床上的应用情况及起不到保护神经的可能性原因。资料来源:应用计算机检索Pubmed数据库2000/2005与神经保护和雌激素有关的文章,检索词为“Estrogen,Neuroprotection,EstrogenReplace-mentTherapy”限定文章语言种类为英文。同期检索维普数据库相关文章,检索词为“神经保护或脑保护、雌激素”。资料选择:对资料进行初审,纳入标准:①关于雌激素神经保护的基础研究方面主要是涉及其神经保护的机制方面的实验研究原著。②关于临床研究的要求是样本量较大的随机双盲对照研究。③关于国内的文献,限定为中药的神经保护作用的研究。排除标准为:重复的研究。资料提炼:共收集449篇文章。排除重复和类似研究,对符合标准的17篇文献进行分析。资料综合:体外细胞培养、组织培养及缺血动物模型方面的研究都表明,雌激素对神经的保护是确定的。它主要通过作用于各种雌激素受体,调控细胞死亡途径中保护性基因而使神经元更能耐受缺血等损伤因素带来的伤害,同时作用于神经胶质细胞等细胞使其表达各种细胞因子而起到保护神经元的作用。当然雌激素的神经保护的机制还有其他的途径。然而在临床上却发现雌激素替代治疗增加了脑卒中的发生率,不能阻止轻度认知功能障碍的发生。导致雌激素替代治疗不能行的原因也许是,没有考虑其他的激素对神经保护的影响,或者没有找到对神经元起到保护作用的更特异性的受体。结论:雌激素在体外的各个方面的研究证实其神经保护作用是确切的,但是在临床随机对照研究却得不到证实,这需要对其作用机制进行进一步的研究。

OBJECTIVE： To investigate the neuroprotective mechanism of estrogen and observe its application in clinic and the reason it cannot protect the brain from damage. DATA SOURCES： A computer-based online search of Pubmed was unertaken to identify the articles about neuroprotection and estrogen published in English from 2000 to 2005 with the key words of ＂estrogen, neuroprotection, estrogen replacement therapy＂. Another search of Vip database was conducted for related articles with the key words of ＂neuroprotection or braitr protection, Estrogen＂ in Chinese. STUDY SELECTION： The articles were selected firstly. Inclusive criteria： ①The basic research about neuropretective effect of estrogen mainly concluded the original articles related to neuroprotective mechanism; ②The clinical research concerned randomized controlled trials with larger sample size; ③Chinese articles should be neuroprotective effects of Chinese medicines. Exclusive criteria： repetitive articles. DATA EXTRACTION： Totally 449 articles were collected. After excluded the repetitive and similar researches, 17 literatures met the inclusive criteria were selected. DATA SYNTHESIS： Many experiments including cell and tissue culture in vitro and animal models of ischemia indicate that estrogen can protect nerve tissues by combining with different estrogen receptors to regulate protective gene expression in cellular death pathways, making neurons tel- erant to damage caused by ischemia or other factors and neurogiia cells express neurotrophic factors, Additionally, there are many other protective mechanisms. However, clinical randomized controlled trims appeal that estrogen replacement therapy increases the incidence of stroke, and cannot inhibit the occurrence of cognitive dysfunction. It may be because we ignore the interaction between the neuroprotection of other hormones, or we have not found the more specific receptor with neuroprotective effect. CONCLUSION： Further research is needed to explain the contradiction between the experiments and clinical randomized controlled trials.