Abstract: Objective :This study aimed to investigate the pathogenesis and treatment of spinal cord injury by constructing a rat model of acute spinal cord injury.Methods:The modified Allen method was used to establish the rat model of moderate spinal cord injury. The pathogenesis of spinal cord injury was determined by detecting the differences in the expression of related signaling pathways and related inflammatory factors before and after induction.By analyzing the differences of gene expression in related signaling pathways and the expression of related inflammatory factors in different groups of rats, the protective effect of drugs on spinal cord injury was proved.Results:The expression of TLRs/MyD88/ NF- B signaling pathway and related inflammatory factors after spinal cord injury were detected by qPCR and western blot. The results showed that the expression of TLR4/NF-ΚB signaling pathway and related inflammatory factors increased significantly after spinal cord injury compared with the control group, and the difference was statistically significant (p < 0.05).The effects of GM1 on the expression of TLRs/MyD88/ NF- B signaling pathway and related inflammatory factors after spinal cord injury were detected by qPCR and western-blot analysis. The results showed that compared with the spinal cord injury group, GM1 intervention significantly inhibited the activation of the TLR4/NF-ΚB pathway and the expression of related inflammatory factors after spinal cord injury, and the difference was statistically significant (p < 0.05).Conclusion: TLR4/NF-ΚB signaling pathway may become a new target for the treatment of secondary SCI.GM1 is a commonly used drug for the treatment of spinal cord injury. It mainly ACTS as a therapy for SCI by inhibiting the TLR4/NF-ΚB signaling pathway.