Dexmedetomidine alleviates microglial activation of neuropathic pain by modulating miR-23a/PDE10A axis in streptozotocin-induced diabetic mice


 Purpose: To elaborate the functional role of dexmedetomidine (DEX) in alleviating microglial activation diabetic neuropathic pain (DNP) and explore involved signaling pathways.
 Methods: The viability BV-2 cells was measured using a commercial kit. Levels interleukin 1β (IL- 1β) tumor necrosis factor-α (TNF-α) were ELISA mRNA target predicted confirmed TargetScan luciferase assay. Protein expression levels determined by western blotting. Diabetes indiced C57BL/6J mice streptozotocin (STZ) antidiabetic parameters evaluated vivo.
 Results: DEX suppressed HG-induced cells. IL-1β TNF-α increased HG-treated cells, but this counteracted following treatment. Phosphorylation p65 (p-p65) upregulated treated with HG, while repressed upregulation. MiR-23a downregulated addition DEX. mimics induction p-p65. Results from assays showed that 3-untranslated region (UTR) PDE10A directly targeted miR-23a. vivo studies miR-23a agomir relieved reduced expressions p-p65 STZ-induced mice, these effects aggravated DEX.
 Conclusion: results show upregulation miR-23a, alleviates reduces inflammatory factors mice. underlying mechanism at least partially mediated PDE10A.