最新研究证实巨噬细胞/小胶质细胞（M/Ms）的稳态对中枢神经系统损伤修复具有重要作用，但具体的作用机制尚未明确。本课题组前期研究发现：脊髓损伤(SCI)后给予锌（Zn2+）可以增加SCI病灶神经元的存活，伴随M/Ms源性细胞因子变化和NF-κB信号通路的活化；焦亡相关蛋白表达减少。因此，我们提出：SCI后Zn2+通过NF-κB信号通路活化M/Ms，从而减少神经元焦亡的发生，促进SCI恢复。本项目拟通过动物和细胞实验来探索SCI后Zn2+与M/Ms活化的关系，以及M/Ms通过焦亡途径影响神经元的病理改变机制，进而促进SCI的修复进程。本项目旨在从一个新的角度（Zn2+激活M/Ms而减少神经元焦亡）来揭示锌疗法治疗SCI的病理机制，为SCI提供一个新的治疗靶点及方案，具有重要的理论意义和临床应用前景。

Recent study demonstrated that macrophage/microglia(M/Ms) homeostasis plays an important role in the repair of central nervous system injury, but the mechanism is still unclear. Our previous researches found that the survival of neurons increases after spinal cord injury by zinc (Zn2+) administration, while the cytokines secreted from M/M also changes, followed by the activation of NF-κB signaling pathway, and the related protein of pyroptosis decreases. Therefore,we hypothesize that Zn2 + activates M/Ms through NF-κB signaling pathway after SCI, reduces the occurrence of neuron pyroptosis and promotes SCI recovery. This project intends to explore the relationship between Zn2+ and M/Ms activation after SCI at animal and cell experimental level，furthermore the pathological changes of neuronal pyroptosis affected by M/Ms activation and the spinal cord injury recovery. This project aims to elucidate the SCI pathological mechanism by zinc therapy in a new way (Zn2+ activates M/Ms to reduce neuronal pyroptosis), provides a new therapeutic target for SCI , which has an important theoretical significance and clinical value.