促进神经轴突再生对脊髓损伤（SCI）治疗有重要意义。Nogo受体（NgR）是抑制轴突再生因子的共同作用靶点，NEP1-40能通过封闭NgR抑制Rho信号通路而促进轴突生长。我们前期用慢病毒载体将NEP1-40导入神经干细胞（NSC)内，分化后的神经元能明显对抗NogoA对轴突生长的抑制作用，并可促进脊髓功能恢复。但Rho通路的一些关键基因表达上调，提示其分化后的神经元轴突生长受不同机制调控。因此设想除了细胞代替作用外，其通过不同机制调控损伤区和自身分化后神经细胞的轴突生长而促进SCI再生修复。本课题拟构建NEP1-40 NSC，体外观察在NogoA干预下其对背根节神经细胞和自身分化后神经元轴突生长的影响，在基因、蛋白质及磷酸化水平对Rho信号通路的关键部位及下游调控生长锥因子进行检测。并将其移植入SCI动物体内，观察脊髓功能恢复情况和Rho信号转导通路变化，探讨其机制。

It has important significance to promote neural axon regeneration for the treatment of spinal cord injury (SCI). Nogo receptors (NgR) is the common targets of axon regeneration factor. NEP1-40 can close Nogo receptors (NgR), but not activate Rho signaling pathways and promote the growth of axons. We use lentivirus transduce NEP1-40 gene into neural stem cells (NSC) and find neurons which has differentiated can obviously against NogoA inhibition for the growth of axons. It can promote the function recovery of SCI. On testing of some key genes of Rho pathways, We found its expression level update. It hint there is an different mechanisms to regulate neurons axon growth which differentiated from NEP1- 40 NSC.We suppose NEP1-40 NSC promote the function recovery of SCI because of promoting axon growth of neurons which differentiated from it and located injuried area through different mechanism In addition to cell  supplement . This topic proposed in vitro observation NEP1 - 40 NSC influence on two kinds of neurons axon under the NogoA intervention. The key parts of Rho signal transduction pathways and regulation of the growth cone downstream factors in the aspect of gene and protein level, degree of phosphorylation were observed.  The spinal cord function recovery and change of the Rho signal transduction pathways were observed after NEP1-40 NSC implantation in SCI animal. It may be found possible mechanisms of promoting the repair of SCI with NEP1-40 NSC.