黄芪对青光眼视神经病变中视网膜胶质细胞活化因子转录表达的影响

项目名称： 黄芪对青光眼视神经病变中视网膜胶质细胞活化因子转录表达的影响

项目编号： No.81202726

项目类型： 青年科学基金项目

立项/批准年度： 2013

项目学科： 医学八处

项目作者： 廖良

作者单位： 北京中医药大学

项目金额： 23万元

中文摘要： 青光眼目前治疗以降眼压为主，但已有证据表明即使眼压控制很好，神经元仍遭受继发的、持续的损伤，即青光眼性视神经病变（GON），防治GON需从其发病机制- - RGCs凋亡着手，胶质细胞活化同时具有视神经损伤和视神经保护两种作用，既是RGCs凋亡的启动因素，又是决定受损RGCs能否得到修复的关键环节，针对胶质细胞的靶向治疗有望通过引导将胶质细胞活化转向视神经保护方向而发挥GON保护作用。黄芪作为补气行水中药的代表，在既往临床和基础研究中证实具有RGCs保护作用，且其抗谷氨酸毒性的作用与唯一具有谷氨酸清除作用的胶质细胞功能类似，结合其补气行水的功能和现代药理学作用机制，我们推测黄芪的RGCs保护作用与调节视网膜胶质细胞有关，我们将通过分析GON病变中胶质细胞相关信号因子的转录表达及黄芪的干预效应，对这一假说进行验证，并进一步明确黄芪视神经保护作用的分子机制。

中文关键词： 黄芪；青光眼；胶质细胞；转录；

英文摘要： Current hypotensive treatment options are not sufficient to block neurodegenerative injury in patients with glaucoma.Progressive degeneration of retinal ganglion cells (RGCs) andtheir axons is the primary cause of glaucomatous visual loss.We focused our efforts on better understanding of the precise pathogenic mechanisms of glaucomatous optic neuropathy(GON).Growing evidence now supports that RGC-glia interactions are critically important for different aspects of GON. Despite their relative protection from glaucomatous injury, glial cells prominently respond to glaucomatous stress when exhibit an activated phenotype.Glia-targeting treatment appears to be a promising strategy that could be directed at regulating the initial glial response, reversing the neurodestructive consequences of glial activation, or regaining glial neurosupportive functions. Radix Astragali, which can benefiting qi for diuresis，has been demonstrated by clinical and experimental research as an neuroprotective herb. We also found Radix Astragali make effect by inhibit the neurotoxic response from excessive glutamate, and this process is very similar with what Müer acts because only this type of cell in retina can generate glutamine synthetase to cleanup glutamate.Based on these reasons, we hypothesize that the effect of Radix Astragali ma

英文关键词： Radix Astragali；glia；glaucomatous optic neuropathy；transcription；