Ginkgetin ameliorates IL-1β-stimulated inflammation via modulating PI3K/AKT/NF-κB cascade in human osteoarthritis chondrocytes.

Osteoarthritis (OA) is a degenerative joint condition characterized by an increased density of the subchondral osseous tissue, cartilage degradation, and synovial membrane inflammation. Ginkgetin, a bioactive compound derived from Ginkgo biloba, exhibits notable anti-inflammatory properties in various disease models. In the current study, we aimed to determine the therapeutic potential of ginkgetin in mitigating IL-1β-induced inflammatory responses in human osteoarthritis chondrocytes. Our findings demonstrated that ginkgetin significantly inhibited the IL-1β-induced production of prostaglandin E2 (PGE2) and nitric oxide (NO). Additionally, ginkgetin downregulated the expression of IL-1β-induced proinflammatory mediators and cartilage-degrading enzymes. Furthermore, ginkgetin attenuated the degradation of key extracellular matrix components, including aggrecan and type II collagen. Mechanistically, ginkgetin exerted its protective effects by markedly suppressing the activation of the PI3K/AKT/NF-κB signaling pathway. Taken together, our findings demonstrated that ginkgetin ameliorates IL-1β-stimulated inflammation via modulation of the PI3K/AKT/NF-κB cascade, underscoring its viability as a promising therapeutic strategy for managing OA.