Dihydromyricetin attenuates neuropathic pain via enhancing the transition from M1 to M2 phenotype polarization by potentially elevating ALDH2 activity in vitro and vivo

摘要: Background Treatment for neuropathic pain as a refractory disease remains unsatisfactory and represents significant clinical challenge. A highly effective drug is thus urgently needed treatment. Dihydromyricetin (DMY) flavonoid with wide range of biological activities. The purpose this research to explore the effects DMY on underlying mechanism its effect. Methods effect was investigated in BV-2 cells lipopolysaccharide (LPS)-induced cells. model established via spared nerve injury (SNI) surgery mice, protein expression level detected Western blot assay. percent M1 M2 phenotype polarization were flow cytometry Immunochemical staining assay also performed measure marker levels aldehyde dehydrogenase 2 (ALDH2) level, mechanical sensitivity evaluated measurement withdrawal threshold. Results We found that promoted transition from upregulated ALDH2 vitro vitro. ALDA-1, an agonist, switching vivo alleviated hypersensitivity induced by SNI enhancing elevating activity mice. After DMY- or ALDA-1-microglia injected into SNI-induced hypersensitive threshold increased significantly when compared group. Conclusions Our data demonstrated potentially vivo. may have alleviative pain. findings herein provide promising avenue treatment, suggesting new target, ALDH2, treatment