国际眼科纵览 ›› 2013, Vol. 37 ›› Issue (1): 59-62.doi: 10.3760/ cma. j. issn.1673.5803.2013.01.011

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氧化损伤在青光眼发病中的作用

吴佳慧  崔红平    

  1. 200120上海,同济大学附属东方医院眼科
  • 收稿日期:2012-10-30 出版日期:2013-02-22 发布日期:2013-02-26
  • 通讯作者: 崔红平,Email:hpcuistar@gmail.com

Effect of oxidative stress in the development of glaucoma 

WU Jia-hui, CUI Hong-ping.   

  1. Department of Ophthalmology, Shanghai East Hospital Affiliated to Tongji University, Shanghai 200120, China
  • Received:2012-10-30 Online:2013-02-22 Published:2013-02-26
  • Contact: CUI Hong-ping, Email: hpcuistar@gmail.com

摘要: 青光眼是一种多因素诱导的视神经退行性病变,其中氧化应激损伤在复杂的青光眼发病机制中的起着重要作用。青光眼的氧化损伤机制可能对眼部的某些组织细胞产生损伤作用,促使细胞内抗氧化物酶作用下降、抗氧化作用相关蛋白增加,最终导致蛋白沉积、细胞死亡。氧化损伤可以导致小梁网细胞线粒体骨架改变,最终使小梁网发生退行性病理改变。氧化损伤还可促使视网膜神经节细胞内抗氧化作用相关蛋白增加、线粒体内源性凋亡,最终导致视网膜神经节细胞功能丧失。(国际眼科纵览,2013,37:59-62)

Abstract: Glaucoma is an irreversible neuropathy and oxidative stress probably plays an important role in its pathological process. Oxidative damage can destroy cells of many parts of ocular tissue, induce decrease of intracellular antioxidant enzymes and increase antioxidantrelated proteins, finally lead to deposition of these proteins and cell death. Oxidative damage also modifies the cytoskeleton of mitochondria in trabecular meshwork cells and causes pathologic degradation of trabecular meshwork cells. Oxidative stress also induces raise of antioxidantrelated proteins and endogenous apoptosis of mitochondria in retinal ganglion cells, and lastly results in retinal ganglion cell dysfunction. (Int Rev Ophthalmol, 2013, 37: 59-62)