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哺乳动物视神经损伤后不能成功再生,除了视网膜神经节细胞再生能力低下外,与中枢神经系统中存在抑制微环境密切相关。少突胶质细胞产生的髓鞘相关抑制分子是构成这种抑制微环境的重要成分。目前已经鉴定的抑制分子主要有 Nogo、髓磷脂相关糖蛋白及少突胶质细胞髓磷脂糖蛋白,他们通过同一受体复合体转导抑制信号。通过阻滞抑制分子及其受体或改变神经元的内在状态,可以克服抑制分子的抑制作用,促进视网膜神经节细胞轴索再生,为人类视神经损伤修复带来希望。
In mammals, the regeneration of the optic nerve can not be successfully regenerated. In addition to the low regenerative capacity of retinal ganglion cells, there is a close correlation with the inhibition of the microenvironment in the central nervous system. Oligodendrocyte-derived myelin-related suppressor molecules constitute an important component of this inhibitory microenvironment. Currently identified suppressor molecules are mainly Nogo, myelin-related glycoprotein and oligodendrocyte myelin glycoprotein, they inhibit signaling through the same receptor complex transduction. By blocking the inhibitory molecules and their receptors or changing the intrinsic state of the neurons, the inhibitory effect of the inhibitory molecules can be overcome and the retinal ganglion cell axon regeneration can be promoted, thereby providing hope for the repair of human optic nerve injury.