Fig. 3

Treatment effect of Dexamethasone (DEX 40nM) on inflamed chondrocytes (proteomics data analysis). (A) DEX treatment led to a decreased abundance of inflammatory mediators such as matrix metalloproteinase − 1 (MMP1, T24: q = 0.746, T48: q = 0.000), matrix metalloproteinase − 3 (MMP3, T24: q = 0.000, T48: q = 0.000) and superoxide dismutase 3 (SOD3, T24: q = 0.072, T48: q = 1.00) compared to inflamed chondrocytes, but DEX treatment significantly increased chitinase-3 like-protein-1 (CH3L1, q = 0.000) at T48 compared to healthy cells. (B) DEX treatment non-significantly improved the secretion of extracellular matrix (ECM) proteins such as aggrecan (ACAN), procollagen C-proteinase enhancer (PCOLCE), hyaluronan and proteoglycan link protein 1 (HAPLIN1) and collagen type VI alpha 1 (COL6a1) compared to inflamed untreated chondrocytes, but their abundance remained significantly lower than in healthy controls at T24 (ACAN, T24: q = 0.048, T48: q = 0.283; PCOLCE, T24: q = 0.050, T48: q = 0.202) or T48 (HAPLIN1, T24: q = 0.349, T48: q = 0.000; COL6A1, T24: q = 0.276, T48: q = 0.048). ns…not significant (p ≥ 0.05), *…p < 0.05, **…p < 0.01, ***…p < 0.001.