Betulinic acid inhibits IL-1β-induced inflammation by activating PPAR-γ in human osteoarthritis chondrocytes

- BA dose-dependently inhibits IL-1β-induced MMP-1, MMP-3, MMP-13, PGE2 and NO productions.
- BA inhibits IL-1β-induced NF-κB activation.
- BA was found to activate PPAR-γ and the inhibition of PGE2 and NO by BA can be reversed by PPAR-γ antagonist GW9662.

Betulinic acid (BA), a triterpenoid isolated from birch bark, has been reported to have anti-inflammatory effects. In this study, we investigated the anti-osteoarthritic effects of BA in IL-1β-stimulated human osteoarthritis chondrocytes. Human osteoarthritis chondrocytes were pre-incubated with BA (6, 12, 24 μM) for 12 h and then treated with IL-1β (10 ng/ml). The production of PGE2 and NO were detected by ELISA and Griess reagent. The expression of NF-κB, IκB, and PPAR-γ were detected by Western blotting. The results showed that BA dose-dependently inhibited IL-1β-induced MMP-1, MMP-3, MMP-13, PGE2 and NO productions. BA also inhibited IL-1β-induced NF-κB activation. Furthermore, BA was found to activate PPAR-γ and the inhibition of PGE2 and NO by BA can be reversed by PPAR-γ antagonist GW9662. In conclusion, these results suggested that BA inhibited IL-1β-induced inflammation in osteoarthritis chondrocytes by activating PPAR-γ.