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Endoplasmic reticulum stress (ERS) has been demonstrated to exhibit a critical role in osteoarthritic chondrocytes. Whether 5,7,3′,4′-tetramethoxyflavone (TMF) plays the chondroprotective role in inhibition of PGE 2 -induced chondrocytes apoptosis associating with ERS has not been reported. To investigate this, the activation of PERK, ATF6, and IRE1 signaling pathways in ERS in chondrocytes pretreated with PGE 2  was studied. By treatment with PGE 2 , the chondrocytes apoptosis was significantly increased, the proapoptotic CHOP and JNK were upregulated, the prosurvival GRP78 and XBP1 were downregulated, and GSK-3 β  was also upregulated. However, TMF exhibited the effectively protective functions via counteracting these detrimental effects of PGE 2 . Finally, the inflammatory cytokine PGE 2  can activate ERS signaling and promote chondrocytes apoptosis, which might be associated with upregulation of GSK-3 β . TMF exhibits a chondroprotective role in inhibiting PGE 2 -induced ERS and GSK-3 β .

The Chondroprotective Role of TMF in PGE2-Induced Apoptosis Associating with Endoplasmic Reticulum Stress

The Chondroprotective Role of TMF in PGE₂-Induced Apoptosis Associating with Endoplasmic Reticulum Stress