Fig. 4. AhR-dependent inhibition of p-AMPKα in mice or hepatocytes treated with alcohol.

a PCA score plot (left) and heatmap of the Pearson correlation matrix (right) based on the hepatic transcriptome data obtained from WT or Ahr HKO mice fed Lieber-DeCarli diet for 5 weeks (n = 3 each; darker green, closer negative correlation; darker red, closer positive correlation). b Heatmap and hierarchical correlation analyses of DEGs using the same data as in (a) (DEGs of P < 0.05 and FC >2). The DEGs were hierarchically clustered and presented as heatmap according to the row Z-score (darker blue, stronger downregulation; darker yellow, stronger upregulation). c Bar graphs based on KEGG analysis to identify functional processes controlled by Ahr HKO using the same data as in (a). FDR and genes are presented as bar graphs (FDR <0.01). d Immunoblots from the liver homogenates obtained from the mice subjected to control or Lieber-DeCarli diets for 5 weeks (left) and their quantifications (right) (n = 5 each). e Representative immunohistochemical images for p-AMPKα using the same mice as in (d) (n = 5 each). Scale bar: 100 μm. f–h Immunoblots in mPHs isolated from the mice fed as in (d) (left) and their quantifications (right) (f; n = 3 each); mPHs treated with 100 mM ethanol for 48 h (left) or AML-12 cells treated with 100 mM ethanol for 48 h after transfection with siAhR (or siCon) for 24 h (right) (g; repeated three times with similar results); mPHs treated with 100 μM kynurenine for 12 h (left) or AML-12 cells treated with 100 μM kynurenine for 12 h after transfection with siAhR (or siCon) for 24 h (right) (h; repeated three times with similar results). Values are expressed as means ± SEM. Significantly different compared to Con or WT. Data were analyzed via one-way ANOVA with Tukey HSD (d, f). Source data are provided as a Source Data file.