Ophiopogonin D Attenuates Mitochondrial Dysfunction in Chondrocytes via Nrf2 Signaling to Ameliorate Osteoarthritis

抄録

Osteoarthritis (OA) is a progressive joint disorder characterized by cartilage degradation, inflammation, and chondrocyte dysfunction, with mitochondrial dysfunction and oxidative stress being central to its pathogenesis. The Nrf2 pathway is vital for maintaining redox homeostasis and mitochondrial integrity. This study investigated the protective effects of Ophiopogonin D (OP-D), a natural saponin compound, on IL-1β-induced chondrocyte injury in vitro. Using C28/I2 cells, we demonstrated that OP-D restored cell viability and reduced the secretion of proinflammatory cytokines following IL-1β exposure. OP-D also alleviated mitochondrial dysfunction by decreasing mitochondrial ROS production and preserving mitochondrial membrane potential. Furthermore, OP-D mitigated extracellular matrix degradation. Mechanistically, OP-D activated the Keap1/Nrf2 pathway. These findings suggest that OP-D exerts chondroprotective effects by improving mitochondrial function and maintaining ECM integrity via Nrf2 pathway activation, highlighting its therapeutic potential for the treatment of osteoarthritis.