摘要
青光眼是一组以视网膜神经节细胞（RGCs）丢失和视野缺损为特征的神经退行性疾病，其病理机制尚不完全清楚，眼压升高被认为是青光眼发生和发展最主要的危险因素。小梁网及Schlemm管是房水引流系统的主要组成部分，其结构或功能异常可引起房水流出的受阻进而引起眼压升高。越来越多的证据表明，氧化损伤可能在人小梁网细胞凋亡、功能障碍及其他退行性改变过程中发挥作用。氧化损伤是体内氧化和抗氧化失衡，从而引起脂质过氧化反应、蛋白质变性、DNA损伤等一系列组织病理损伤的过程。既往研究发现青光眼患者房水中氧化应激标志物水平升高，且氧化应激可引起小梁网细胞DNA氧化损伤、细胞内线粒体氧化损伤和炎症反应。本文就氧化应激在小梁网功能损伤中发挥的作用及可能的机制进行综述。
Glaucoma is a group of neurodegenerative disease characterized by progressive retinal ganglion cells （RGCs） death and visual field defect. Although its pathological mechanism is unclear, elevated intraocular pressure is considered to be the main contributing factor. As the main components of the aqueous humor drainage system,the structural abnormalities, dysfunction of trabecular meshwork and Schlemm canals may cause aqueous humor outflow obstruction and result in elevated intraocular pressure. Increasing evidences suggest that oxidative stress is the key factor leading to the apoptosis,dysfunction of the human trabecular meshwork cell,and other progression of degenerative changes. Oxidative damage is an imbalance between the oxidative stress and anti-oxidative system, which leads to lipid peroxidation,protein denaturation and DNA damage. Previous studies showed that the level of oxidative biomarker was elevated in the aqueous humor of glaucoma patients. In addition,oxidative stress is thought contributing to the pathogenesis of DNA damage,mitochondrial dysfunction and inflammation in human trabecular meshwork cells. This review considered the contribution of oxidative stress on human trabecular mesh work dysfunction and its possible mechanisms.
出处
《中华实验眼科杂志》
CAS
CSCD
北大核心
2016年第4期375-379,共5页
Chinese Journal Of Experimental Ophthalmology
关键词
氧化应激
小梁网
青光眼
Oxidative stress
Trabecular meshwork
Glaucoma
