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实验性青光眼中载有胶质细胞源性神经营养因子的可生物降解微球对视网膜神经节细胞的神经保护作用

Neuroprotection of retinal ganglion cells with GDNF-Loaded biodegradable microspheres in experimental glaucoma.

作者信息

Xiao Jian-He, Zhang Mao-Nian

机构信息

Department of Ophthalmology, the Chinese PLA General Hospital, Beijing 100853, China.

出版信息

Int J Ophthalmol. 2010;3(3):189-91. doi: 10.3980/j.issn.2222-3959.2010.03.01. Epub 2010 Sep 18.

Abstract

Glaucoma is the second leading cause of blindness worldwide, and also the most common optic neuropathy. The ultimate cause of vision loss in glaucoma is thought to be retinal ganglion cell (RGC) death. Neuroprotection of RGC is therefore an important goal of glaucoma therapy. Currently, glaucoma treatment relies on pharmacologic or surgical reduction of intraocular pressure (IOP). It is critical to develop treatment approaches that actively prevent the death of RGCs at risk in glaucoma. Neurotrophic factors have the ability to promote the survival and influence the growth of neurons. Neurotrophic factor deprivation has been proposed as one mechanism leading to RGC death in glaucoma. Effective neuroprotection in glaucoma likely requires the consistent availability of the active agent for prolonged periods of time. Biodegradable microspheres are especially attractive as drug delivery vehicles for a number of reasons. Sustained GDNF delivery by biodegradable microspheres offers significant neuroprotection to injured RGC in experimental glaucoma. PLGA microsphere-delivered GDNF represents an important neuroprotective strategy in the treatment of glaucomatous optic neuropathy and provides direction for further investigations of this hypothesis.

摘要

青光眼是全球第二大致盲原因,也是最常见的视神经病变。青光眼导致视力丧失的最终原因被认为是视网膜神经节细胞(RGC)死亡。因此,对RGC的神经保护是青光眼治疗的一个重要目标。目前,青光眼治疗依赖于通过药物或手术降低眼压(IOP)。开发能够积极预防青光眼高危RGC死亡的治疗方法至关重要。神经营养因子具有促进神经元存活和影响其生长的能力。神经营养因子剥夺被认为是导致青光眼RGC死亡的一种机制。青光眼的有效神经保护可能需要长时间持续提供活性剂。由于多种原因,可生物降解微球作为药物递送载体特别有吸引力。可生物降解微球持续递送胶质细胞源性神经营养因子(GDNF)为实验性青光眼中受损的RGC提供了显著的神经保护。聚乳酸-羟基乙酸共聚物(PLGA〕微球递送的GDNF是治疗青光眼视神经病变的一种重要神经保护策略,并为进一步研究这一假说提供了方向。

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