Fig. 2

Loss of AKR1A1 exacerbates alcohol-induced liver injury and inflammation. After the treatments, the survival rates (A) were recorded, and western blot analyses of hepatic AKR1A1 expression (B), serum assays of ALT (C) and AST (D) levels, hepatic triglyceride content assays (E), IHC staining for hepatic AKR1A1 expression (F), H&E staining of the liver tissue sections (G), western blot analyses of hepatic IL-1β and TNF-α levels (H), and qRT‒PCR examination of hepatic IL-1β and TNF-α mRNA levels (I) were performed. The data were compared between WT and Akr1a1^−/− mice receiving the PF and AF treatments. The quantification of the western blot and qRT‒PCR was performed by β-actin normalization, and the relative protein and mRNA expression were compared to the PF-treated WT mice in folds. Data are represented as the means ± SD (n = 6). 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)