Fig. 4.

CTGF activated the NF-κB and AP-1 through ASK1-p38/JNK pathways. a RA cells were incubated with 10 ng/ml CTGF or TGF-β1 for 24 h, and total protein extracts were collected. The expression of key molecules in ASK, p38/JNK, and NF-κB/AP-1 pathways and their phosphorylation states were examined by Western blotting. b RA cells were treated with either 10 μM ASK1 inhibitor GS-4997, or solvent control as indicated, for 30 min prior to stimulation with 20 ng/ml CTGF for 24 h. The expression of ASK, p65, and c-Jun and their phosphorylation states were examined by Western blotting. c RA cells were treated with either 5 μM SB20358 or 25 μM SP600125, or DMSO as control, for 30 min prior to stimulation with CTGF for 24 h, and total protein extracts were collected. The expression of ASK, p65, c-Jun and their phosphorylation states were examined by Western blotting. d RA cells were treated with chemical inhibitors or solvent control for 30 min prior to stimulation with 10 ng/ml CTGF for 24 h. The mRNA expression of IL-6 was analyzed using qRT-PCR. *p < 0.05 and **p < 0.01 as compared with CTGF group.