姜黄素通过调控TXNIP-NLRP3信号通路缓解骨关节炎症损伤与细胞凋亡OA

Objective This study aimed to investigate the protective effects of curcumin on lipopolysaccharide(LPS)-induced osteoarthritic inflammatory damage and its underlying molecular mechanisms.Methods Primary murine articular chondrocytes were cultured in vitro and pretreated with varying concentrations of curcumin(10,20,and 40 µmol/L)before LPS stimulaltion to establish an inflammation-induced injury model.The levels of inflammatory cytokines IL-1β,IL-18,and TNF-α in the cell supernatant were measured using enzyme-linked immunosorbent assay(ELISA).Western blot analysis was performed to assess the protein expression levels of TXNIP,NLRP3,and Caspase-1.The number of ASC specks and the apoptosis rate of chondrocytes were observed using confocal microscopy.Additionally,a murine osteoarthritis model was established via sodium iodoacetate(MIA)induction,and real-time quantitative PCR(qPCR)was utilized to evaluate the protective effects of curcumin on articular cartilage.Results Curcumin inhibited LPS-induced inflammatory cytokine secretion in a dose-dependent manner.Mechanistically,curcumin was found to bind to TXNIP,thereby suppressing the activation of the NLRP3 inflammasome,leading to a reduction in ASC speck formation and chondrocyte apoptosis.In vivo experiments demonstrated that intraperitoneal administration of curcumin(20 mg/kg)alleviated knee joint inflammation in osteoarthritic mice.Conclusion Curcumin mitigates osteoarthritic inflammation and chondrocyte apoptosis by inhibiting the activation of the TXNIP-NLRP3 signaling pathway,suggesting its potential as a therapeutic target for osteoarthritis treatment.