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

07:00 EST 16th December 2019 | BioPortfolio

Summary of "Dexmedetomidine attenuates LPS-mediated BV2 microglia cells inflammation via inhibition of glycolysis."

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 neuro-protective 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 up-regulation of sirt1 expression, inhibited HIF-1α expression and glycolysis, thus reducing LPS-mediated inflammation in BV2 cells.


Journal Details

This article was published in the following journal.

Name: Fundamental & clinical pharmacology
ISSN: 1472-8206


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