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几乎所有视神经病变的最后通路均为视网膜神经节细胞(retinal ganglion cell,RGC)的凋亡。视神经损伤后RGC的凋亡滞后,且在相当长的时间内仍有RGC幸存,说明损伤后RGC凋亡并没有立即启动,可能有其他抵抗因子在发挥作用。因此,研究RGC幸存机制并最终找到视神经保护治疗的新方法具有重要意义。当前,轴突损伤后视神经保护治疗仍以预防RGC凋亡为主,对RGC保护的介绍很少涉及内源性机制,本文主要就内源性RGC的保护机制和一些对视神经有保护作用的内源性因子进行综述。
Almost all the pathological changes of optic nerve are the apoptosis of retinal ganglion cell (RGC). The apoptosis of RGCs lagged after optic nerve injury, and RGC survived for a long time, indicating that RGCs apoptosis did not start immediately after injury, and other resistance factors may play a role. Therefore, the study of RGC survival mechanism and ultimately find a new method of optic nerve protection therapy is of great significance. Currently, optic nerve protection after axonal injury is still the prevention of RGC-based apoptosis, the introduction of RGC protection is rarely involved in endogenous mechanisms, this paper mainly on the protection of endogenous RGC and some of the protective effect of the optic nerve within Source of factors are reviewed.