4.7 Article

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

Journal

INTERNATIONAL IMMUNOPHARMACOLOGY
Volume 25, Issue 1, Pages 83-87

Publisher

ELSEVIER SCIENCE BV
DOI: 10.1016/j.intimp.2015.01.018

Keywords

Astragalin; Osteoarthritis; NF-kappa B; IL-1 beta

Funding

  1. National Natural Science Foundation of China [81272015]
  2. Heilongjiang Postdoctoral Fund [LBH-Z12189]

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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 astmgalin on IL-1 beta-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-kappa B and MAPKs was detected by western blot analysis. We found that astragalin dose-dependently inhibited IL-1 beta-induced NO and PGE2 production, as well as iNOS and COX-2 expression. Meanwhile, western blot analysis showed that astragalin inhibited IL-1 beta-induced NF-KB and MAPK activation in human osteoarthritis chondrocyte. In addition, astragalin was found to activate PPAR-gamma. The inhibition of astragalin on IL-1 beta-induced NO and PGE2 production can be reversed by PPAR-gamma antagonist GW9662. Astragalin suppressed IL-1 beta-induced inflammatory mediators via activating PPAR-gamma, which subsequently inhibited IL-1 beta-induced NF-kappa B and MAPK activation. Astragalin may be a potential agent in the treatment of osteoarthritis. (C) 2015 Elsevier B.V. All rights reserved.

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