Fig. 4

PPAR-γ agonists inhibit TGF-β1-induced fibrogenic activation of human intestinal myofibroblasts. a–f HIFs were treated with TGF-β1 (5 ng/ml) co-incubated with or without PPAR-γ agonists (A, C, E: TRG; B, D, F: RSG) for 24 h. a, b Representative RT-PCRs show the mRNA expression of collagen1A1 (Col1A1), fibronectin (FN), and α-SMA, with GAPDH as the endogenous control. c, d Representative Western blots show the protein expression of procollagen1A1 (Procol1A1), FN, and α-SMA, with β-Actin as the endogenous control. e, f Plots of relative protein expression of Procol1A1, FN, and α-SMA normalized to densitometric values obtained in cells stimulated with only 5 ng/ml TGF-β1. Data are the means ± SD averaged for three (E) or four (F) independent experiments. ^# P < 0.05 versus control group; ^## P < 0.01 versus control group; *P < 0.05 versus TGF-β1 only group; **P < 0.01 versus TGF-β1 only group. Data were analyzed by one-way ANOVA followed by Tukey’s post hoc test