Phillygenin inhibits inflammation in chondrocytes via the Nrf2/NF-κB axis and ameliorates osteoarthritis in mice

Abstract

Objective

Osteoarthritis (OA), widely seen in the elderly, is featured by cartilage degradation, subchondral bone remolding, and synovium inflammation. Currently, there is no cure for OA development. Phillygenin (PHI), an active ingredient from the Forsythiae Fructus, possesses many biological properties, such as anti-inflammation and anti-oxidative stress in several diseases. However, the potential effects and underlying mechanisms of PHI on OA remain unclear.

Methods

Western blotting, RT-PCR, ELISA and tissue staining were employed to explore the mechanisms by which PHI exerted a protective effect on IL-1β-induced production of pro-inflammation cytokines and extracellular matrix (ECM) degradation in primary murine chondrocytes and destabilization of the medial meniscus (DMM) mouse models.

Results

In this study, we found that PHI inhibited the production of pro-inflammation cytokines and ECM degradation induced by IL-1β in primary murine chondrocytes. Mechanically, PHI inhibited the NF-κB pathway via activating nuclear factor (erythrluteolind-derived 2)-like 2 (Nrf2). In vivo experiments also confirmed the chondroprotection of PHI in DMM mouse models.

Conclusion

PHI alleviated IL-1β-induced inflammation cytokines and ECM degradation via activating Nrf2 and inhibiting NF-κB pathway.

The translational potential of this article

This study provides a biological rationale for the use of PHI as a potential candidate for OA treatment.

Graphical abstract