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. 2018 Dec 18;8:17939. doi: 10.1038/s41598-018-36063-2

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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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Hypoxia induces HIF-1α, CHOP and apoptosis in rat lung exposed to hypoxia. Lungs of rats stabulated in normoxia (Nx) (21% of O₂) or exposed to hypoxia (Hx) (8% FiO₂-like) during 24 h, 48 h or 72 h were used for immunohistochemistry, TUNEL assay, apoptosis enzymatic assay and RT-qPCR analysis. Paraffin-embedded rat lung serial sections were immunostained for HIF-1α or CHOP and counterstained with nuclear fast red. Original magnification: X400 (A). Rat lung sections have been TUNEL-labeled (green) (shown by arrow) and DAPI-stained (blue). Original magnification: X200, scale bars represent 100 μm (B). The activity of effector caspase 3 was evaluated by enzymatic assay in rat lung homogenates (C). Bim mRNA expression levels were evaluated in rat lung homogenates by RT-qPCR (D). n = 6–8 rats per group. Data were submitted to a Kruskal-Wallis one-way analysis of variance followed by a Dunn’s multiple comparison tests with *P < 0.05 representing a significant difference as compared with normoxic condition.