Abstract
MicroRNAs have been reported to be an important pathophysiological factor in neuropathic pain. However, the potential mechanism through which miRNAs function in neuropathic pain remains unclear. The purpose of this study was to explore the potential role of mir-34c in neuropathic pain in a mouse model of chronic constriction injury (CCI). We found that overexpression of miR-34c greatly alleviated CCI-induced neuropathic pain and spinal cord infarction, and reduced cell apoptotic and inflammatory cytokine expression in CCI mice. We also demonstrated that miR-34c suppressed the expression of NLRP3 by directly binding the 3′-untranslated region. Overexpression of miR-34c decreased the protein levels of NLRP3, ASC, caspase-1, IL-1β, and IL-18 in the spinal cord in CCI mice. Together, our results indicated that miR-34c may inhibit neuropathic pain development in CCI mice through inhibiting NLRP3-mediated neuroinflammation.
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