Abstract

NLRP3 is a member of the NOD-like family of adaptive immune responses that recognize both exogenous damage-associated molecular patterns and endogenous damage-related molecular patterns. NLRP3 recognizes that PAMPS/DAMPS is activated, binds to ASC and Caspase-1 to form NLRP3 inflammatory vesicles, and exerts immunity in pathogenic infectious diseases and autoimmune diseases by controlling the release of IL-1β and IL-18, but The role of peripheral nerve injury is not clear. The objective of this study is to investigate the effect of NLRP3 on repair after sciatic nerve injury. This study was divided into two parts. The first part established the sciatic nerve injury model. In the second part, NLRP3 intervention was given on the basis of the sciatic nerve injury model. The results showed that The model of sciatic nerve injury in mice was established successfully. The sciatic nerve function of the MSU group and the MCC950 group recovered better than the control group, and the recovery of the MCC950 group was the best. It is concluded that moderate inhibition of nlrp3-mediated inflammatory response is helpful for peripheral nerve repair after injury.

Highlights

  • Peripheral nerves are mainly composed of somas embedded in the spinal cord, brain stem, dorsal root ganglia, sympathetic ganglia, or parasympathetic ganglia and extended axons that signal with target organs[1]

  • 1.3.2 IL-1β mRNA level in mouse sciatic nerve Compared with the sham operation group, IL-1β mRNA expression level was significantly increased in the model group 24 h after surgery (P < 0.001)

  • 2.3 Results 2.3.1 IL-1β mRNA and caspase-1 mRNA levels in mouse sciatic nerve Compared with the control group, the expression level of il-1 mRNA in the mcc950 group was significantly lower at 4 hours after operation, and the difference was statistically significant (P

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Summary

Introduction

Peripheral nerves are mainly composed of somas embedded in the spinal cord, brain stem, dorsal root ganglia, sympathetic ganglia, or parasympathetic ganglia and extended axons that signal with target organs[1]. Pathological changes such as nerve conduction interruption, intra-neuronal edema, and Waller degeneration occur after peripheral nerve injury. Regeneration after peripheral nerve injury is a complex process influenced by many factors, and the microenvironment of the nerve after injury is an important influencing factor. Innate immunity regulates the microenvironment after peripheral nerve injury by releasing various cytokines and signal transduction effects, thereby affecting regeneration after peripheral nerve injury. The most representative inflammasome is nucleotide binding domain-like receptor protein(NLRP3)[5]

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