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. 2023 Sep 29;11:e16155. doi: 10.7717/peerj.16155

Figure 4. FXR suppresses fibrosis in P-MC via downregulation of Smad3 and upregulation of Smad7 expression.

Figure 4

(A, B) After treatment with TGF β1 (five ng/mL) for 24 h in FXR+/+ mice (A) and FXR−/− mice (B), P-MCs were treated with CDCA (100 nM) or DMSO for another 24 h. Then, the mRNA expression of collagen I, CTGF, TGF β1, FXR, SHP, Smad3, and Smad7 were determined by qRT-PCR (n = 3), and the protein expression of fibrosis factors, FXR, SHP, p-Smad3/Smad3, and Smad7 were determined by Western blot (n = 3).∗P < 0.05,∗∗P < 0.01, ∗∗∗P < 0.001 vs. TGF β1-CDCA; #P < 0.05,##P < 0.01,###P < 0.001 vs. TGF β1+CDCA. (C, D) After treatment with adv-FXR α2 (10 MOI) or GFP for 24 h in FXR+/+ mice, P-MCs were treated with TGF β1 (five ng/mL) for another 24 h. Then, the mRNA expression of collagen I, CTGF, TGF β1, Smad3, and Smad7 were determined by qRT-PCR (n = 3) (C), and the protein expression of fibrosis factors, p-Smad3/Smad3, and Smad7 (D) were examined by Western blot (n = 3).∗P < 0.05, ∗∗∗P < 0.01, ∗∗∗P < 0.001 vs. Ctrl adv-GFP; #P < 0.05,##P < 0.01,###P < 0.001 vs. adv-GFP.