Dexmedetomidine attenuates LPS‐mediated BV2 microglia cells inflammation via inhibition of glycolysis

Abstract Microglia inflammation induces pro‐inflammatory cytokines and pro‐inflammatory enzymes expression, thus leading to inflammation‐mediated neuronal cell death. Increased intracellular glycolysis participates in LPS‐mediated microglia inflammation. Dexmedetomidine exhibits neuroprotective effects in some situations. In this study, we mainly focused on whether and how dexmedetomidine inhibits LPS‐mediated cellular glycolysis and inflammation in BV2 cells. LPS induced pro‐inflammatory cytokines and pro‐inflammatory enzymes expression, and increased glycolysis capacity in BV2 cells. Moreover, inhibition of glycolysis by 2DG attenuated LPS‐induced pro‐inflammatory cytokines and pro‐inflammatory enzymes expression. Moreover, LPS upregulated hypoxia‐inducible factor 1α (HIF1α) expression and decreased sirt1 expression. Dexmedetomidine counteracted these effects induced by LPS. Further, 2‐methoxyestradiol, a HIF1α inhibitor, could inhibit LPS‐mediated glycolysis and inflammation in BV2 cells, which was similar to the effects of dexmedetomidine. In addition, these effects of dexmedetomidine could be reversed by EX527, a sirt1 inhibitor. The present study indicated that dexmedetomidine, via upregulation of sirt1 expression, inhibited HIF‐1α expression and glycolysis, thus reducing LPS‐mediated inflammation in BV2 cells.