MicroRNA-193a Downregulates HMGB1 to Alleviate Diabetic Neuropathic Pain in a Mouse Model

Background: Diabetic neuropathy is a serious complication for diabetic patients involving the nervous system. This disease is a quiet but painful condition caused by chronically high blood glucose levels. It is reported that high mobility group box 1 protein (HMGB1) participates in the development of neuropathic pain. This study aimed to explore the role of microRNA (miR)-193a in diabetic neuropathic pain through the regulation of HMGB1. Methods: A diabetic mouse model was established through the injection of streptozocin (STZ). Neuropathic pain development was shown by paw withdrawal thresholds and paw withdrawal latency. Expression levels of relative genes or miR were analyzed by qRT-PCR, while Western blot was employed to assess the protein levels. The interaction between miR-193a and HMGB1 mRNA 3 '-UTR region was shown by luciferase assay. The levels of inflammation cytokines were measured by ELISA kits. Results: miR-193a expression was decreased and HMGB1 expression was upregulated in the lumbar spinal dorsal horn of STZ-induced diabetic mice. miR-193a inhibited HMGB1 expression in the lumbar spinal dorsal horn. Overexpression of miR-193a alleviated neuropathic pain in STZ-induced diabetic mice. Peripheral neuroinflammation in diabetic mice was suppressed by miR-193a overexpression. Conclusion: This research illustrates that miR-193a alleviates diabetic neuropathic pain in a mouse model through the inhibition of HMGB1 expression.