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0 reviewsAbstractOxidative stress-induced chondrocyte damage is a key contributor to the progression of osteoarthritis (OA). While trigonelline (TG) possesses anti-infammatory and antioxidant activities, its functional role and underlying mechanisms in OA remain unclear. In this study, the human chondrocyte cell line CHON-001 was treated with TG alone or in combination with IL-1β or ML385 for 24 h. Chondrocyte injury-related events were assessed using Cell Counting Kit-8 (CCK-8), fow cytometry with Annexin V-FITC/PI kit, Hoechst staining, the probe 2,7-Dichlorofuorescin diacetate (DCFH-DA), SA-β-gal staining, and SOD and MDA assay kits. Our data revealed that TG alleviated IL-1β-induced infammation, apoptosis, extracellular matrix (ECM) degradation, senescence, and oxidative stress in chondrocytes, accompanied by the downregulation of Keap1 and upregulation of Nrf2, HO-1 and NQO1. ML385 treatment reversed the protective efects of TG against IL-1βinduced injury in chondrocytes. In vivo, the anterior cruciate ligament transection (ACLT) was used to induce a rat OA model, and TG was administered by gavage. OA severity and articular cartilage degradation were evaluated by hematoxylin and eosin (H&E), toluidine blue, Safranin-O staining, and Osteoarthritis Research Society International (OARSI) scoring system. The in vivo data showed that TG attenuated the degeneration and erosion of articular cartilage, suppressed infammation, and downregulated the levels of Keap1 and iNOS, while upregulating the levels of Nrf2 and Col2a1. In conclusion, our study demonstrated that TG inhibits oxidative stress-induced chondrocyte dysfunction and cartilage degradation by activating the Keap1/Nrf2/ARE signaling pathway.