视神经炎（ON）是中青年人主要致盲性眼病，与视神经脊髓炎（NMO）密切相关。促进病灶处髓鞘的修复及再生是治疗疾病和改善预后的关键，而SDF-1/CRCX4信号通路是调控髓鞘修复再生的重要通路。我们前期临床研究发现，脑脊液中SDF-1浓度与NMO相关视神经炎患者预后密切相关；通过我们创新性动物模型研究发现，该信号通路参与调控NMO炎性脱髓鞘病变髓鞘修复再生。我们认为SDF-1/CXCR4信号通路是通过调控少突胶质前体细胞(OPCs)的存活、迁移、增殖及分化过程来促进髓鞘修复再生，但具体作用机制尚不明确。本研究首次研究SDF-1/CXCR4信号通路在NMO-IgG诱导的炎性脱髓鞘病灶中的调控作用机制，拟从动物实验及细胞实验两方面，进一步证实其在NMO炎性脱髓鞘病变中的作用，明确其调控OPCs的作用机制；探索CNS炎症诱导局部髓鞘修复的起点及下游信号通路，具有较好的科学创新性和显著临床应用价值。

Optic neuritis (ON) is one of the most common ophthalmological diseases, which mostly occurs in young adults and the middle aged. ON always occur as the first symptom of neuromyelitis optica (NMO) in Asia. Neuromyelitis optica is an inflammatory demyelinating disorder of the CNS. Failure of axon ensheathment and loss of neural function are extensively observed in NMO lesions due to a loss of oligodendrocytes. Remyelination failure may be attributed to impaired recruitment and arrested differentiation of endogenous OPCs. It is reported that modulating the SDF-1/CXCR4 chemokine axis during the pathological process might benefit remyelination by enhancing OPC recruitment and differentiation. Our recent study has demonstrated that NMOSD patients with a lower CSF level of SDF-1 and higher AQP4 autoantibody level usually had a poor recovery after treatment when compared with those with higher SDF-1 level. Using SDF-1 and the CXCR4 antagonist AMD3100, combined with in vitro cell research, this study intends to evaluate rats’ motor function, demyelinated histopathological features and cellular and molecular biologic changes. The aim of this study is to understand the mechanisms responsible for repair of damaged myelin, which is critical for developing therapies that promote remyelination and prevent disease progression.