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. 2018 Oct 2;8:14652. doi: 10.1038/s41598-018-32376-4

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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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Simvastatin inhibited apoptosis in rat myocardial tissue in LPS induced inflammation detected by TUNEL staining, magnification 400x. Brown stained nuclei indicate TUNEL-positive cardiomyocytes. The apoptosis increased significantly in the LPS (b) and simvastatin group (c) compared with the control group (a). Note that induction of sepsis by LPS resulted in a marked appearance of TUNEL-positive cardiomyocytes (arrow) quantified and shown as AIs (black columns) (e), which was significantly reduced by simvastatin 20 (c) and simvastatin 40 (D). (e) Quantitative analysis of apoptotic cells counted in immunohistochemically stained myocardial sections for cleaved caspase 3 and corresponding frequencies of TUNEL positive cardiomyocytes are shown, *p < 0.01 in comparation with LPS group, **p < 0.05 in comparation with simvastatin 20, ^#p < 0.05 in comparation with LPS group.