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. 2018 Sep 19;8:14019. doi: 10.1038/s41598-018-32411-4

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© The Author(s) 2018

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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Hydrogen gas (HG) prevented steatotic primary hepatocyte apoptosis when hepatocytes were subjected to hypoxia/reoxygenation (H/R). (A) Expressions of Sirt1, HO-1, Bax, Bcl-2, cleaved caspase-3, and caspase-3 from steatotic primary hepatocytes after hypoxia/reoxygenation (H/R) injury which was suppressed by hydrogen gas (HG) was detected by western blot analysis. β-actin was used as a loading control. Representative blot (up) and quantified protein levels (down) are shown. Data are expressed as the means ± SEM; *p < 0.05, **p < 0.01. Data are representative of three independent experiments and indicate the mean ratio of triplicate results from each experiment.