lncRNA MALAT1 contributes to neuropathic pain development through regulating miR-129-5p/HMGB1 axis in a rat model of chronic constriction injury.

Mounting studies pay attention to the functional roles of long non-coding RNAs (lncRNAs) in many human diseases including neuropathic pain. LncRNA MALAT1 has been indicated to serve as a critical mediator in neuropathic pain with unclear mechanisms. The present study aims to explore the functional roles of MALAT1 in neuropathic pain progression and the related mechanisms. Bilateral sciatic nerves were ligated to induce chronic constriction injury (CCI) in order to establish the neuropathic pain rat model followed by behavioral tests, RT-qPCR, Western blotting, and ELISA. Dual luciferase activity assay was performed to determine the binding effect between MALAT1 or HMGB1 and miR-129-5p. The mRNA levels of MALAT1 were significantly enhanced in CCI rats. MALAT1 inhibition repressed the development of neuropathic pain and neuroinflammation. Additionally, miR-129-5p was decreased and HMGB1 was increased, both of which could be rectified by MALAT1 inhibition. Meanwhile, MALAT1 targeted miR-129-5p/HMGB1 axis. Finally, miR-129-5p suppression attenuated the inhibitory effect of MALAT1 inhibition on neuropathic pain and neuroinflammation development in CCI rats. The present study demonstrates that MALAT1 might modulate neuropathic pain targeting miR-129-5p/HMGB1 axis. These findings may lead to a promising and efficacious clinical approach for the treatment of neuropathic pain.