Galangin attenuates IL-1β-induced catabolism in mouse chondrocytes and ameliorates murine osteoarthritis.

OBJECTIVE

Osteoarthritis (OA) is one of the most common chronic diseases, which is characterized by cartilage degeneration, subchondral osteosclerosis, and synovitis. Accumulating evidence has shown that galangin, a flavonoid derived from medicinal herbs, exhibits numerous pharmacological activities in various diseases. This study aimed to investigate the effects of galangin on interleukin (IL)-1β-induced inflammation in mouse chondrocytes and explore the underlying mechanisms.

METHODS

In this study, we investigated the protective effects of galangin on IL-1β-induced inflammatory response in vitro using the CCK-8 assay, RT-qPCR, western blotting, and immunofluorescence staining. In addition, the therapeutic effects of galangin on the anterior cruciate ligament transection (ACLT) mouse model were also explored in vivo.

Results

Galangin treatment suppressed the expression of IL-1β-induced inflammatory cytokines, such as nitric oxide synthase, cyclooxygenase-2, TNF-α, and IL-6. Furthermore, galangin attenuated hypertrophic conversion and the extracellular matrix degradation via inhibiting the expression of catabolic enzymes. Mechanistically, galangin inhibited the activation of the JNK and ERK MAPK pathways and nuclear factor kappa-B (NF-κB) signaling pathway. In addition, galangin treatment ameliorated cartilage degeneration in an OA model in vivo.

Conclusion

Galangin suppressed the IL-β-induced inflammatory response in vitro and ameliorated cartilage degeneration in vivo via inhibiting the NF-κB pathway and JNK and ERK pathways, suggesting its potential as an effective candidate for the treatment of OA.