Neuropathic pain (NP) continues to be a significant problem that lacks effective treatment. Our study sought to explore a new promising gene target for the treatment of NP. Differential and enrichment analyses were performed on 24,197 genes and 12,088 genes from the NP microglial microarray and sequencing dataset. Candidate differentially expressed genes (DEGs), functions, and signaling pathways that are closely related to NP were identified by analyzing the bioinformatic results. For in vivo experiments, mice were divided into the sham and NP groups. The expressions of DEGs were validated to screen out the NP hub genes. For in vitro experiments, the hub genes in resting M0-BV2 and polarized M1-BV2 microglia were examined by immunofluorescence, flow cytometry, and qRT-PCR. DEGs in the NP microarray and sequencing data shared five candidate genes, CD244, MEGF9, PCGF2, PLSCR1, and NECAB2. The results of the in vivo experiment showed that the NP model group exhibited higher expression of PLSCR1 and MEGF9 compared to the sham group. The enrichment results of the DEGs revealed the biological processes of "response to lipopolysaccharide". PLSCR1 was highly expressed in the lipopolysaccharide-induced M1-BV2 microglia. PLSCR1 is a potential gene associated with microglial polarization in NP. These findings provide a new view on understanding the pathogenesis mechanism of NP.
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