Fig. 6

Expression of p-ERK and p-Akt in IL-1β-treated human OA chondrocytes. A Cells pretreated WY14643 (50 μM) for 2 h were co-treated with IL-1β (10 ng/ml) for 22 h. The expression of Akt, p-Akt, ERK, p-ERK, and β-actin protein levels were detected via western blotting; B cells were pretreated with WY14643 (50 μM), U0126 (20 μM), WY14643 (50 μM) + U0126 (20 μM) and WY14643 (50 μM) + TCN (10 μM) for 2 h, respectively, and were then co-treated with IL-1β (10 ng/ml) for 22 h. GAG levels were measured via Dimethylmethylene blue assay; C cells were pretreated with WY14643 (50 μM), U0126 (20 μM) or WY14643 (50 μM) + U0126 (20 μM) for 2 h, respectively, and were then co-treated with IL-1β (10 ng/ml) for 22 h. The expression of ERK, p-ERK, Collagen II, Aggrecan, MMP13, ADAMTS5, P62, LC3B, Beclin1, Bcl2, and β-actin protein levels were detected via western blotting; D cells were pretreated with WY14643 (50 μM), TCN (20 μM) or WY14643 (50 μM) + TCN (10 μM) for 2 h, respectively, and were then co-treated with IL-1β (10 ng/ml) for 22 h. The expression of Akt, p-Akt, Collagen II, Aggrecan, MMP13, ADAMTS5, P62, LC3B, Beclin1, Bcl2, and β-actin protein levels were detected via western blotting. The data are representative of three independent experiments (*p < 0.05)