摘要
目的:原发性开角型青光眼(POAG)是一种发病隐匿的不可逆性致盲性眼病,发病机制有待进一步探讨。本研究通过激光共聚焦显微镜及流式细胞方法检测鱼藤酮对青光眼患者小梁细胞氧化损伤的影响,探讨POAG的发病机理。方法:原代培养POAG患者及正常人小梁网细胞,采用激光共聚焦显微镜、流式细胞技术观察不同浓度鱼藤酮对小梁网细胞内ROS水平的影响。结果:原代POAG患者小梁网细胞内ROS水平明显高于正常人,差异有统计学意义(P<0.05)。ROT对GTM小梁网细胞ROS的诱导作用呈时间-浓度依赖性,而正常人原代小梁网细胞NTM经过ROT处理后,结果显示ROT浓度高于5μmol/L时对正常人小梁网细胞内ROS产生有显著诱导作用(P<0.01);而≤5μmol/L时,ROT对NTM细胞内ROS的产生并没有明显诱导作用。在不同浓度下,ROT对原代POAG患者和正常人小梁网细胞ROS的诱导作用相比,均有显著性差异(P<0.01)。结论:鱼藤酮诱导小梁网氧化损伤增强,提示线粒体复合物活性下降可能会引起青光眼患者小梁网功能障碍,推测其与眼压升高及POAG发病密切相关。
Objective： Primary open angle glaucoma （POAG） is a kind of insidious disease which results in irreversible loss of vision. The mechanism of POAG needs further investigation. The aim of this study is to explore the pathogenesis of POAG by the degeneration of trabecular meshwork（TM） using electron microscope （EM） method. Methods： TM from POAG （GTM） and non-diseased individuals （NTM） were cultured in vitro. Comparison of mitochondria and cell junction in TM cells were observed through transmission EM.Results： There were many complete mitochondria in the cytoplasm of NTM cells. Main cell junction was gap junction which has complete structure between NTM ceils. Massive rough endoplasmic reticulum and few Golgi apparatus were seen. In GTM cells, number of mitochondria is decreased with incomplete structure. Normal cell junction was hardly seen. Other cell organdies were also decreased. Conclusions： The abnormalities of cell junction and mitochondrial morphology in TM cells may cause the dysfunction oftrabecular meshwork, which was closely related with the elevated intraocular tension and the mechanism of POAG.
出处
《中国伤残医学》
2012年第8期24-26,共3页
Chinese Journal of Trauma and Disability Medicine
基金
国家自然科学基金项目(No.81100665)
陕西省科技厅项目(2011K14-02-07)
陕西省卫生厅项目(2010D56)
陕西省教育厅项目(2010JK807)
西安医学院校级项目资助
