Regulation of cell apoptosis by Silybinin targeting the TLR4/NF-κB pathway improves cartilage injury in a rat model of knee osteoarthritis

XU Tian-bo; LIU De-guo; ZHANG Jie-hong; LYU Ao; HOU Zhen-hai

doi:10.13820/j.cnki.gdyx.20232950

Abstract：Objective To investigate the effect of silybinin(SB)on cartilage injury in a rat model of knee osteo-arthritis(KOA)and explore its impact on the Toll-like receptor 4(TLR4)/nuclear factor-κB(NF-κB)pathway and cell apoptosis.Methods SD rats were divided into a normal control group,model group,and SB group,with 8 rats in each group(total n=24).The KOA model was established by intra-articular injection of papain,followed by 6 weeks of SB intervention.Histological changes were observed using safranin O-fast green and hematoxylin-eosin staining,and histological scoring was performed using the Osteoarthritis Research Society International(OARSI)scoring system.West-ern blot was used to detect the expression changes of TLR4,NF-κB,p65,BAX,BCL-2,and Caspase-3 proteins.Results The OARSI score of the knee joint cartilage tissue in the model group was significantly higher than that in the normal control group(P＜0.000 1).Additionally,the levels of TLR4,NF-κB,p65,BAX,and Caspase3 proteins in the subchondral bone tissue of the model group were significantly increased,while the expression level of the anti-apop-totic protein BCL-2 was significantly decreased(P＜0.000 1).Compared with the model group,the OARSI score of the joint cartilage tissue in the SB group was significantly lower(P＜0.001),and the expression levels of TLR4,NF-κB,p65,BAX,and Caspase3 proteins in the subchondral bone tissue were significantly downregulated,while the expression level of BCL-2 was significantly upregulated(P＜0.000 1).Conclusion Silybinin inhibits cell apoptosis by suppress-ing the activation of the TLR4/NF-κB pathway in subchondral bone,thereby repairing cartilage injury in the rat model of KOA.