Resveratrol protection against IL-1β-induced chondrocyte damage via the SIRT1/FOXO1 signaling pathway

Purpose Osteoarthritis (OA) is a common joint disease characterized by cartilage degeneration, synovial inflammation, osteophytes, and subchondral osteosclerosis. This study investigated the effects of resveratrol (RES) on extracellular matrix (ECM), autophagy, and apoptosis in OA pathogenesis via the SIRT1/FOXO1 pathway. Methods The microenvironment of OA chondrocytes was stimulated in vitro by adding 10 ng/mL of IL-1 beta to primary Wistar rat chondrocyte. Western blotting, immunofluorescence, quantitative real-time PCR, and transmission electron microscopy (TEM) were used for analysis. Results In the presence of IL-1 beta, RES increased the expression of silent information regulator (SIR) 1 protein and the phosphorylation level of forkhead transcription factor (FOXO) 1. It also promoted chondrocyte autophagy, increased the expression of SOX9 and aggrecan, inhibited chondrocyte apoptosis and matrix breakdown, and protected chondrocytes from IL-1 beta damage. After a SIRT1 inhibitor or FOXO1 inhibitor was added, the protective effect of RES on chondrocytes was significantly weakened. Our results suggest that RES regulates the ECM metabolism, autophagy, and apoptosis of OA chondrocytes through the SIRT1/FOXO1 pathway to ameliorate IL-1 beta-induced chondrocyte injury. Conclusion RES protects chondrocytes from IL-1 beta-induced damage by activating SIRT1/FOXO1 signaling and holds potential in OA treatment.

Automated summary

This study shows that resveratrol regulates the pathogenesis of osteoarthritis through the SIRT1/FOXO1 pathway, promoting chondrocyte autophagy, inhibiting apoptosis and matrix breakdown, and protecting chondrocytes from damage.