Fig. 5.

Sal attenuated TNF-α-driven inflammation in human chondrocytes via inhibition of NF-κB signaling. (A–C) The levels of NO, PGE2, and IL-6 in the culture medium of human OA chondrocytes pretreated with Sal at different concentrations and stimulated with 20 ng/ml TNF-α. (D, E) The levels of iNOS and COX-2 in human chondrocytes pretreated with Sal at different concentrations and stimulated with 20 ng/ml TNF-α. (F, G) Cytoplasmic IκBα and nuclear p65 levels in human chondrocytes pretreated with Sal at different concentrations and stimulated with 20 ng/ml TNF-α. (H) The nuclear translocation of p65 was detected using immunofluorescence combined with DAPI staining of nuclei (scale bar: 20 µm). All results are presented as the means ± SDs of six duplicate experiments. ^##P < 0.01 compared to the control group; *P < 0.05, **P < 0.01 compared to the TNF-α alone group.