科研之友
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摘要
MicroRNA (miRNA) are emerging as critical regulators of neuropathic pain development. Neuroinflammation contributes to the development of neuropathic pain. miR-142-3p has been characterized as an inflammation-related miRNA in various pathological processes. However, little is known about the role of miR-142-3p in neuroinflammation and neuropathic pain. The present study aimed to investigate the function of miR-142-3p in neuropathic pain by creating a murine model using spinal nerve ligation (SNL). A significant reduction in miR-142-3p expression was observed in the dorsal root ganglion of mice with SNL (P<0.05) compared with control mice. Overexpression of miR-142-3p significantly inhibited neuropathic pain and neuroinflammation in mice with SNL (P<0.05). High mobility group box 1 (HMGB1) was identified as a direct target gene of miR-142-3p by bioinformatic analysis and dual-luciferase reporter assays. Overexpression of miR-142-3p significantly reduced the mRNA and protein expression levels of HMGB1 in vitro and in vivo (P<0.05). In addition, HMGB1 mRNA expression and miR-142-3p expression were inversely correlated in mice with SNL. Furthermore, overexpression of HMGB1 significantly reversed the inhibitory effect of miR-142-3p on neuroinflammation and neuropathic pain development (P<0.05). Overall, these results suggest that miR-142-3p functions as a negative regulator of neuropathic pain development through the downregulation of HMGB1, indicating that miR-142-3p may serve as a potential therapeutic target for neuropathic pain.
