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

Int Immunopharmacol

Department of Orthopedic Surgery, the Second Hospital of Harbin Medical University, Harbin, Heilongjiang Province 150086, People's Republic of China. Electronic address:

Published: March 2015

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.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.intimp.2015.01.018DOI Listing

Publication Analysis

Top Keywords

human osteoarthritis
12
osteoarthritis chondrocyte
12
nf-κb mapk
12
mapk activation
12
inhibited il-1β-induced
12
astragalin
9
il-1β-induced inflammatory
8
inflammatory mediators
8
activation astragalin
8
inos cox-2
8

Similar Publications

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!