Fig. 3

Loss of AKR1A1 aggravates alcohol-induced hepatocyte oxidative damage. The liver tissues were subjected to qRT‒PCR examination of the expression of Nox-2 (A), Sod-1 (B), Nqo-1(C), Caspase 3 (D), and Caspase 8 (E) and biochemical assays of MDA (F), GSH (G), and GSSG (H) levels. The calculated hepatic GSSG/GSH ratio is shown in Panel (I). The liver tissue sections were also subjected to IHC staining for the detection of 4-HNE (J). In addition, western blot analysis was performed to examine the hepatocellular ADH, ALDH2, CYP2E1, and 4-HNE levels (K). Data are presented 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)