Fig. 4

Long-term implications of Dexamethasone (DEX) (40nM and 1µM) treatments. (A) All conditions proliferated significantly slower (p < 0.0001) compared to healthy untreated over a period of 9 days. (B) Intracellular reactive oxygen species (ROS) levels significantly increased in inflamed (p = 0.0169) compared to healthy chondrocytes. DEX treatment did not reverse ROS accumulation in inflamed cells (40nM p = 0.8795, 1µM p = 0.4403), leaving ROS levels of DEX treated inflamed cells significantly higher than in healthy controls (40nM p = 0.0162, 1µM p = 0.0412). DEX treatment had no significant effect on ROS levels of healthy chondrocytes (40nM p = 0.1741, 1µM p = 0.0818). (C) SA-β Gal activity significantly increased in healthy chondrocytes treated with DEX (40nM:p = 0.0411 and 1µM:p = 0.0078) compared to healthy untreated chondrocytes. Neither inflammation (p = 0.3310) nor DEX treatment of inflamed chondrocytes (40nM:p = 0.8390, 1µM:p = 0.7526) increased SA-β Gal activity compared to healthy chondrocytes. (D) Caspase 3/7 activity significantly decreased in inflamed (p = 0.0401) but not in healthy (p = 0.5299) chondrocytes treated with DEX 1µM compared to healthy controls. Neither inflammation itself (p = 0.6766) nor DEX treatment 40nM significantly altered caspase 3/7 activity in either inflamed (p = 0.1282) or healthy (p = 0.9497) chondrocytes. ns…not significant (p ≥ 0.05), *…p < 0.05, **…p < 0.01, ***…p < 0.001.