Fig. 3.

Improvement of TAA-induced liver fibrosis by p300 inhibitors. (A) Experimental design to investigate the anti-fibrotic effects of p300 inhibitors on TAA-induced mouse liver fibrosis. Vehicle (0.01% DMSO 100 μl), C646 (5 mg/kg), and A6 (5 mg/kg) were administered intraperitoneally 3 times a week for 2 weeks in TAA-injected mice (n = 5). Saline was used for control. (B) Serum AST and ALT levels of TAA-treated mice with or without p300 inhibitors (n = 5). (C) Average ratio of liver weight to body weight of TAA-injected mice with vehicle, C646, or A6 (n = 5). (D, E) Representative photomicrographs of liv-er tissues (D) and percentages (E) of Sirius red staining, MTS, and IHC analysis of αSMA from TAA-treated mice with or without p300 inhibitors (n = 5). (F) Western blot analysis of p300, αSMA, and COL1A in liver tissues from mice treated with TAA with or without p300 inhibitors. β-actin was used as the sample loading control. (G) RT-qPCR expression analysis of fibrosis marker genes ACTA2(αSMA), TNC, Col1a1, Col3a1, and CTGF in the liver of TAA-treated mice with or without p300 inhibitors at 2 weeks after TAA injection. Data are represented as mean ± SEM, *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001 by ordinary one-way ANOVA test.