TMF protects against chondrocyte apoptosis and extracellular matrix degradation by activating SOCS3 expression in osteoarthritisOA

Objective:Osteoarthritis(OA)is characterized by chronic inflammation and cartilage destruction.Chondrocyte,the unique cell type in the cartilage,is responsible for the maintenance of extracellular matrix(ECM)homeostasis.Chondrocyte dysfunction may disrupt ECM homeostasis,induce cartilage destruction,and promote OA development.Suppressor of cytokine signaling 3(SOCS3)negatively plays a critical role in inflammation.This study aims to investigate whether 5,7,3'',4''-tetramethoxyflavone(TMF)inhibited chondrocyte apoptosis and ECM degradation by activating SOCS3 expression.Methods:C28/I2 cells were stimulated by interleukin-1β(IL-1β)to establish OA-like chondrocyte models.Flow cytometry was used to detect chondrocyte apoptosis.Lentivirus infection was employed to knockdown SOCS3 expression.Western blotting and immunofluorescent assays were used to determine the protein expression.Results:IL-1βtreatment induced chondrocyte apoptosis,up-regulated matrix metalloproteinase-13(MMP-13)expression,and down-regulated CollagenⅡexpression.In addition,the expression of SOCS3 was attenuated in IL-1β-treated chondrocytes.TMF could effectively reverse the effects of IL-1βon chondrocytes.SOCS3 knockdown could abolish the effects of TMF on IL-1β-treated chondrocytes.Conclusion:TMF could inhibit OA chondrocyte apoptosis and suppress ECM degradation by activating SOCS3 expression.