Recently, microRNAs are reported to be participated in the development of pain and persistence of neuropathic and inflammatory pain in animal models. Here, we characterized the functional role of miR-129-5p in pain processing in chronic constriction injury (CCI) rat models. Bilateral CCI operation was used to generate neuropathic pain rat model. Paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) were used to assess pain-related behaviors. Gene expression was evaluated using qRT-PCR, luciferase assay, western blotting, and enzyme-linked immunosorbent assay. Compared with the control rats, expression level of miR-129-5p was downregulated significantly over time in CCI rats post operation. Interestingly, downregulation of miR-129-5p in CCI rats was correlated with increased proinflammatory cytokine expression and pain-related behaviors. Furthermore, we found that miR-129-5p alleviated neuropathic pain through downregulating high mobility group protein B1 (HMGB1) expression in CCI rats as overexpression of miR-129-5p suppressed expression of both HMGB1 and proinflammatory cytokine and alleviated pain sensation in CCI rats. In summary, our results show that alteration in miR-129-5p expression contributes to pain processing in our CCI pain rat model, suggesting miR-129-5p could be a causal factor in neuropathic pain and serve as a promising potential biomarker and therapeutic target for neuropathic pain.
Keywords: CCI rat models; Cytokines; HMGB1; Neuropathic pain; miR-129-5p.