Capillarisin Suppresses Lipopolysaccharide-Induced Inflammatory Mediators in BV2 Microglial Cells by Suppressing TLR4-Mediated NF-κB and MAPKs Signaling Pathway.

Abstract

Capillarisin, one of the major bioactive compounds derived from Artemisia capillaries Thunb, has been reported to have extensive pharmacological properties, such as ant-inflammatory and anti-nociceptive activities. However, the molecular mechanisms responsible for the anti-inflammatory activity of capillarisin have not been elucidated in microglia. In the present study, we investigated the anti-inflammatory effects and molecular mechanisms of capillarisin on LPS-stimulated BV2 microglial cells. The effects of capillarisin on inflammatory mediators TNF-α, IL-6, IL-1β, NO and PGE2 were detected. The effects of capillarisin on NF-κB and MAPK activation were detected by western blotting. The results showed that capillarisin suppressed LPS-induced TNF-α, IL-6, IL-1β, NO and PGE2 production in a dose-dependent manner. Capillarisin also inhibited LPS-induced TLR4 expression, NF-κB and MAPKs activation in BV2 microglia. In conclusion, capillarisin inhibited LPS-induced inflammation by blocking TLR4-mediated NF-κB and MAPKs activation in BV2 microglia.