Quercitrin attenuates the progression of osteoarthritis via inhibiting NF-κB signaling pathways and enhance glucose transport capacity

Osteoarthritis (OA) is a common musculoskeletal disorder that impairs function and reduces the quality of life. Extracellular matrix (ECM) degradation and inflammatory mechanisms are crucial to the progression of OA. In this study, we aimed to investigate the anti-inflammatory activity, anti-ECM degradation property, and glucose transport capacity of quercitrin (QCT) on IL-1 beta-treated rat primary chondrocytes. Rat primary chondrocytes were treated with IL-1 beta to simulate inflammatory environmental conditions and OA in vitro. We examined the effects of QCT at concentrations ranging from 0 to 200 mu M on the viability of rat chondrocytes and selected 5 mu M for further study. Using qRT-PCR, immunofluorescent, immunocytochemistry, and western blotting techniques, we identified the potential molecular mechanisms and signaling pathways that are responsible for these effects. We established an OA rat model through anterior cruciate ligament transection (ACLT). The animals were then periodically injected with QCT into the knee articular cavity. Our in vivo and in vitro study showed that QCT could inhibit IL-1 beta-activated inflammation and ECM degradation in chondrocyte. Furthermore, QCT could inhibit the NF-kappa B signal pathway and enhance glucose transport capacity in the IL-1 beta-stimulated chondrocytes. In vivo study proved that QCT attenuates OA progression in rats. Overall, QCT inhibited the activation of NF-kappa B and enhanced glucose transport capacity to alleviate the progression of OA.