Fig. 5

Loss of AKR1A1 aggravates alcohol-induced liver fibrosis. After the treatments, Masson’s trichrome (A) and Sirius red (B) staining were performed in the liver tissue sections to evaluate the effects of AKR1A1 loss on alcohol-induced liver fibrosis. Scale bar = 100 μm. The expression of fibrosis-related marker genes, including Tgf-β1 (C), Col1a1 (D), Ctgf (E), and α-sma (F), was examined by qRT–PCR. The relative mRNA levels were quantified by β-actin normalization and expressed in relation to the PF-treated WT mice. Furthermore, western blot analysis of the phosphorylated p53 (p-p53) and the total p53 in the liver tissues is shown in Panel (G). The relative p53 activation was quantified by determining the intensity ratio between p-p53 and p53 and subsequently comparing with the PF-treated WT mice. Data are presented as the means ± SD (n ≥ 5). Statistical differences were marked as follows: ^#p < 0.05, ^##p < 0.01, ^###p < 0.001 (compared with the PF-treated WT group); *p < 0.05, **p < 0.01, ***p < 0.001 (compared between the other groups)