视神经损伤的保护策略研究现状

Research progress on protective strategies for optic nerve injury

外伤性视神经病变和青光眼可引起视神经退行性改变,进而导致视力显著下降,严重影响患者的生活质量。近年来,通过对哺乳动物视神经损伤模型的研究发现,视神经损伤涉及细胞凋亡、炎症反应和氧化应激等病理生理过程。研究人员对视神经损伤的相关机理和调控信号通路进行了深入探索,并且在对抗视网膜神经节细胞(RGC)凋亡、新型药物治疗、基因治疗、干细胞移植以及天然提取物等方面进行了视神经损伤的保护研究。研究表明热休克蛋白70家族的成员葡萄糖调节蛋白75以及人体视网膜中自然分泌的褪黑素可能在RGC凋亡调控中起重要作用。人粒细胞集落刺激因子(G-CSF)可能通过直接激活内在的G-CSF受体和下游信号通路而起到保护RGC的作用。另外,基因治疗因具有很高的靶向性,有望成为视神经损伤后修复和再生的有效疗法。脂肪干细胞移植能够抵抗大鼠模型中视网膜细胞的凋亡。此外,枸杞多糖可以延迟轴突的继发变性,可能成为延缓视神经损伤继发性变性有前景的天然提取物。本文将对视神经损伤的相关机制、调控及保护途径作一综述。

Traumatic optic neuropathy and glaucoma can cause optic nerve degenerative changes leading to a significant decline in vision,which seriously affects the quality of life of patients.In recent years,research on mammalian optic nerve injury models has found that optic nerve injury involves pathophysiological processes such as apoptosis,inflammatory response,and oxidative stress.Researchers have explored the relevant mechanisms and regulatory signaling pathways of optic nerve injury,and have conducted research on the protection of optic nerve injury in the fight against retinal ganglion cell(RGC)apoptosis,new drug therapy,gene therapy,stem cell transplantation and natural extracts.Studies have shown that glucose regulatory protein 75,a member of the heat shock protein 70 family,and melatonin naturally secreted in the human retina may play an important role in the regulation of RGC apoptosis.Human granulocyte colony-stimulating factor(G-CSF)may play a protective role in RGC by directly activating the intrinsic G-CSF receptor and downstream signaling pathway.Targeting gene therapy is expected to become a powerful therapy for repair and regeneration of injured optic nerve.Adipose stem cell transplantation can resist the apoptosis of retinal cells in rat model.In addition,lycium barbarum polysaccharide can delay the secondary degeneration of axons,which may be a promising natural extract to delay the secondary degeneration of optic nerve injury.This article summarized the mechanism,regulation and protection of optic nerve injury.