轴突再生困难是脊髓损伤不愈的关键，促进轴突生长、突触连接是当前研究的热点之一。研究表明，M2a型巨噬细胞可促进成熟感觉神经元的轴突再生，但其发生机制尚未阐明；基于巨噬细胞被IL-4激活为M2a亚型时Arginase1的表达显著增高；且Arginase1是促进神经元的细胞支架构成与轴突再生的重要开关分子。因此，我们推测M2a型巨噬细胞可通过上调Arginase1的表达，激活神经元的Cdc42信号通路，促进细胞支架构成，从而达到轴突再生的作用。为此，本项目拟通过体外损伤神经元和脊髓挫伤大鼠模型，采用RNA干扰、免疫组化、实时定量PCR、Western-blot等技术，从分子、细胞及整体不同水平明确Arginase1在介导M2a巨噬细胞促进轴突再生中的作用及相关分子机制，为临床治疗脊髓损伤提供新的靶点。

Axonal regeneration is the key of therapy for spinal cord injury. Promote axonal growth and synaptic connectivity is one of focus issues. Research shows that M2a can promote axonal regeneration of mature sensory neurons, but its mechanism has not been elucidated. Meanwhile arginase1, an important molecular switch on promote neurons scaffold constitute and axonal regeneration, was significantly increased by M2a activation. Therefore, we speculate that M2a could promote neuron axonal regeneration by up-regulation the expression of Arginase1 to activate Cdc42 signaling pathway. In this project, after the models of neuronal injury and rat spinal cord contusion are made, the effect and molecular mechanism of Arginase1 mediated M2a promote axonal regeneration are claritied by the methods of iRNA, immunohistochemistry, qPCR and Western-blot. The aim of the project is to provide a new targets for clinical treatment of spinal cord injury.