论文部分内容阅读
青光眼是一种由青光眼性视神经病变引起视野缺损并最终致盲的眼病.青光眼性视神经损伤主要表现为视网膜神经节细胞(RGCs)的死亡,其危险因素除眼压升高之外,还有很多非眼压因素,如神经营养因子剥夺、兴奋性毒性反应、氧化应激反应、小胶质细胞活性增高等参与,非眼压因素所致的青光眼性视神经损害在正常眼压性青光眼的发病中尤为突出.目前,治疗青光眼的主要目的是通过手术和药物降低患者的眼压,以保护患眼的视神经功能,但临床实践发现,部分患者虽然眼压得到了有效地控制,青光眼性视神经病变仍持续进展,提示我们针对青光眼性视神经病变的非眼压致病因素的药物研究对视神经的保护性治疗至关重要.就近年来研发的视神经保护性治疗方法及其机制进行综述.“,”Glaucoma is the second leading cause of blindness worldwide.It is mainly caused by glaucomatous optic neuropathy characterized by retinal ganglion cells (RGCs) loss,which leads to visual field loss and blindness.There are many risk factors other than intraocular pressure (IOP) elevation are thought to be responsible for RGCs damage induced by glaucoma,such as neurotrophic factors deprivation,excitotoxicity,oxidative stress and enhanced microglia activity,and these factors are essential for glaucomatous optic neuropathy,especially in normal tension glaucoma (NTG).Up to date,the major attempt of glaucoma therapy is to protect optic nerve function by lowering IOP through surgery and drugs.However,the therapies can not arrest RGCs damage although effectively lowing IOP in a number of patients.Novel study is turning to find and develop some new approaches to solve neuroprotection problem targeting to the pathogenic factors of glaucomatous optic neuropathy out of IOP.This review paper mainly focused on the neuroprotective therapies that are developed in the past few years.