Objective To investigate whether curcumin(CUR)can reduce chondrocyte inflammation and cartilage degradation in osteo-arthritis(OA)and the underlying mechanisms.Methods A rat model of OA was established.Rats were randomly divided into a Sham,OA,CUR+OA,and deferoxamine(DFO)+OA groups with 10 mice in each group.Chondrocytes from 5-day-old SD rats were divided into the control,interleukin-1β(IL-1β),CUR+IL-1β,and DFO+IL-1β groups.A CCK-8 assay was performed to assess the effects of CUR on cell viability alone or combined with IL-1β.Toluidine blue staining and alcian blue staining were used to observe the morphological changes of IL-1β-induced chondrocytes.The expression of inflammatory response-related proteins(COX-2 and iNOS),extracellular matrix degradation-related proteins(COL2A and MMP13),and p53,SLC7A11,and GPX4 proteins during ferroptosis were detected by Western blotting.The mitochondrial membrane potential was detected by JC-1 staining.Mitochondrial morphology was observed using transmission electron microscopy.Safranine O-fast green/HE staining was performed on cartilage tissues.Immunohistochemical staining was performed to detect COL2A and SLC7A11 expression levels.Results CUR and DFO were found to reduce IL-1β-induced inflammation,cartilage degradation,and ferroptosis,and restore mitochondrial function in chondrocytes.CUR also reversed IL-1β-induced changes in collagen Ⅱ,p53,SLC7A11,GPX4,MMP13,iNOS,and COX-2 levels.In vivo,intra-articular injection of CUR significantly improved cartilage injury in the OA rat model,and the percentages of COL2A-and SLC7A11-positive cells significantly increased in the CUR+OA and DFO+OA groups.Conclusion CUR inhibits ferroptosis and ameliorates cartilage degeneration in OA through p53 signaling pathway.

Objective To investigate whether curcumin(CUR)can reduce chondrocyte inflammation and cartilage degradation in osteo-arthritis(OA)and the underlying mechanisms.Methods A rat model of OA was established.Rats were randomly divided into a Sham,OA,CUR+OA,and deferoxamine(DFO)+OA groups with 10 mice in each group.Chondrocytes from 5-day-old SD rats were divided into the control,interleukin-1β(IL-1β),CUR+IL-1β,and DFO+IL-1β groups.A CCK-8 assay was performed to assess the effects of CUR on cell viability alone or combined with IL-1β.Toluidine blue staining and alcian blue staining were used to observe the morphological changes of IL-1β-induced chondrocytes.The expression of inflammatory response-related proteins(COX-2 and iNOS),extracellular matrix degradation-related proteins(COL2A and MMP13),and p53,SLC7A11,and GPX4 proteins during ferroptosis were detected by Western blotting.The mitochondrial membrane potential was detected by JC-1 staining.Mitochondrial morphology was observed using transmission electron microscopy.Safranine O-fast green/HE staining was performed on cartilage tissues.Immunohistochemical staining was performed to detect COL2A and SLC7A11 expression levels.Results CUR and DFO were found to reduce IL-1β-induced inflammation,cartilage degradation,and ferroptosis,and restore mitochondrial function in chondrocytes.CUR also reversed IL-1β-induced changes in collagen Ⅱ,p53,SLC7A11,GPX4,MMP13,iNOS,and COX-2 levels.In vivo,intra-articular injection of CUR significantly improved cartilage injury in the OA rat model,and the percentages of COL2A-and SLC7A11-positive cells significantly increased in the CUR+OA and DFO+OA groups.Conclusion CUR inhibits ferroptosis and ameliorates cartilage degeneration in OA through p53 signaling pathway.