MiR-23b regulation of metabolites in neuropathic pain: A novel approach.

Abstract

BACKGROUND: MiR-23b has been shown to be involved in a range of neurological disorders and in regulating inflammation and metabolism. However, studies on the role of miR-23b in neuropathic pain (NP) are limited. This study aimed to investigate whether miR-23b could enhance the progression of NP by regulating metabolites. METHODS: Mechanical and thermal pain thresholds were determined in sham, CCI (chronic constriction injury), and KO-CCI mice. Hematoxylin and eosin staining was used to observe morphological changes in the sciatic nerve. Untargeted metabolomics was employed to analyse the changes in metabolic levels in the serum. Furthermore, a significantly decreased metabolite, betaine, was administered intraperitoneally to both sham and CCI mice to determine its effect on the activation level of microglia using immunofluorescence staining. RESULTS: After the knockout of miR-23b, the paw withdrawal threshold and thermal threshold significantly decreased, indicating an exacerbation of pain and increased infiltration of inflammatory cells in the sciatic nerve. Metabolomic analysis revealed alterations in various metabolites following the miR-23b gene knockout. Following betaine treatment, the activation level of microglia in CCI mice showed a decline. CONCLUSION: This study shows that removing miR-23b notably affects metabolic levels, worsening NP in CCI mice. It also explores the possible therapeutic roles of miR-23b in NP.