Astragalin inhibits IL-1β-induced inflammatory mediators production in human osteoarthritis chondrocyte by inhibiting NF-κB and MAPK activation

Astragalin, a bioactive component isolated from Rosa agrestis, has been described to exhibit anti-inflammatory activity. The aim of this study was to investigate the anti-inflammatory effects and the underlying mechanisms of astragalin on IL-1β-stimulated human osteoarthritis chondrocyte. The production of NO and PGE2 was detected by Griess reaction and ELISA. The expression of iNOS and COX-2 was detected by western blotting. The expression of NF-κB and MAPKs was detected by western blot analysis. We found that astragalin dose-dependently inhibited IL-1β-induced NO and PGE2 production, as well as iNOS and COX-2 expression. Meanwhile, western blot analysis showed that astragalin inhibited IL-1β-induced NF-κB and MAPK activation in human osteoarthritis chondrocyte. In addition, astragalin was found to activate PPAR-γ. The inhibition of astragalin on IL-1β-induced NO and PGE2 production can be reversed by PPAR-γ antagonist GW9662. Astragalin suppressed IL-1β-induced inflammatory mediators via activating PPAR-γ, which subsequently inhibited IL-1β-induced NF-κB and MAPK activation. Astragalin may be a potential agent in the treatment of osteoarthritis. •Astragalin inhibits IL-1β-induced NO and PGE2 production.•Astragalin suppresses the expression iNOS and COX-2 both in mRNA and protein levels.•Astragalin inhibits IL-1β-induced NF-κB and MAPK activation in human osteoarthritis chondrocyte.