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. 2018 Feb 23;68(4):708–720. doi: 10.1136/gutjnl-2017-315123

Figure 2.

Figure 2

Inhibition of FoxO1 in patients with AH or ALD animal models. (A) K-mean cluster and gene ontology analyses using the liver samples of patients with AH. FoxO1 was predicted as an inhibitor of alcohol-induced cell death among the most highly differentially expressed genes in GEO dataset (GSE28619). Blue, underexpression; red, overexpression (left). The genes were selected in the categories of two gene ontology pathways (P<0.05) associated with transcriptional regulation and programmed cell death (right). (B) qRT-PCR assay for FOXO1 in the liver of patients with AH (n=5 or 12 each). Each point represents one sample, and the horizontal line does the mean value. (C) qRT-PCR assay for FoxO1 in the liver of mice subjected to binge alcohol drinking (n=7 each). Data were shown as box and whisker plot. Box, IQR; whiskers, 5–95 percentiles and horizontal line within box, median. (D) Immunoblottings for FoxO1 and FoxO3a in the livers from the Lieber-DeCarli or binge alcohol animal models. AH, alcoholic hepatitis; ALD, alcoholic liver disease; Con, control; EtOH, ethanol treatment; FoxO1, forkhead box protein O1; GEO, Gene Expression Omnibus; mRNA, messenger RNA; qRT, quantitative reverse transcription.