GADD45A induces neuropathic pain by activating P53 apoptosis pathway in mice.

Abstract

BACKGROUND: Neuropathic pain is a common condition with current heights of varying etiology. The therapeutic drugs are also poorly work and often limited by side effects such as dizziness. OBJECTIVE: This study aimed to explore the function mechanism of GADD45A in neuropathic pain. METHODS: The DEGs in neuropathic pain mouse model chip were screened by bioinformatics analysis. The expression of GADD45A in SNL model was determined by RT-qPCR and Immunofluorescence assay. The protein expression of p53-apoptosis pathway proteins was determined by western blotting. RESULTS: Combination analysis of bioinformatics methods revealed that the expression of GADD45A was upregulated in SNL. The results of RT-qPCR assay and Immunofluorescence assay revealed that GADD45A was overexpressed in all of time points SNL model. Furthermore, knockdown of GADD45A in SNL remarkably antagonized the malignance phenotype compared with the Ad-GFP treated SNL. In addition, knockdown of GADD45A downregulated the expression of p53 and reduced the apoptosis of spinal cord nerve cells. CONCLUSIONS: Our study suggests that GADD45A may be a biomarker in the neuropathic pain of mice.