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. 2017 Aug 21;7:8976. doi: 10.1038/s41598-017-02759-0

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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ALOX15 knockout attenuated alcohol-induced liver injury, ROS production, ER stress, and apoptosis. WT and ALOX15^−/− male mice were fed with control (PF) or alcohol (AF) liquid diet for 8 weeks. (A) Plasma ALT and AST. (B) Liver histopathological changes shown by H&E staining (arrows: necrosis, arrowheads: lipid droplets). (C) Representative images of 4-HNE staining (upper panel) and DHE staining (lower panel). (D) Immunoblot of proteins involved in ER stress. (E) Immunoblot of proteins involved in apoptosis. Protein levels were quantitated by NIH image J. All values are denoted as means ± SD (n = 6 in A, n = 3 in D and E). Significant differences were indicated by different letters (ANOVA, P < 0.05). *P < 0.05, **P < 0.01, ns, not significant (t-test). H&E: hematoxylin and eosin staining, 4-HNE: 4-hydroxynonenol, DHE: Dihydroethidium, CV: central vein, PV: portal vein.