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

Int Immunopharmacol. 2015 Mar;25(1):83-7. doi: 10.1016/j.intimp.2015.01.018. Epub 2015 Jan 28.

Abstract

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.

Keywords: Astragalin; IL-1β; NF-κB; Osteoarthritis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Anilides / pharmacology
  • Anti-Inflammatory Agents / pharmacology*
  • Cells, Cultured
  • Chondrocytes / drug effects*
  • Chondrocytes / immunology
  • Cyclooxygenase 2 / genetics
  • Cyclooxygenase 2 / metabolism
  • Dinoprostone / metabolism
  • Extracellular Signal-Regulated MAP Kinases / metabolism*
  • Humans
  • Interleukin-1beta / immunology
  • Kaempferols / pharmacology*
  • Middle Aged
  • NF-kappa B / metabolism*
  • Nitric Oxide / metabolism
  • Nitric Oxide Synthase Type II / genetics
  • Nitric Oxide Synthase Type II / metabolism
  • Osteoarthritis / drug therapy*
  • Osteoarthritis / immunology
  • PPAR gamma / antagonists & inhibitors
  • Rosa / immunology*
  • Transcriptional Activation / drug effects

Substances

  • 2-chloro-5-nitrobenzanilide
  • Anilides
  • Anti-Inflammatory Agents
  • Interleukin-1beta
  • Kaempferols
  • NF-kappa B
  • PPAR gamma
  • Nitric Oxide
  • astragalin
  • NOS2 protein, human
  • Nitric Oxide Synthase Type II
  • Cyclooxygenase 2
  • Extracellular Signal-Regulated MAP Kinases
  • Dinoprostone