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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 increased NF-κB expression in rat myocardial tissue in LPS induced inflammation. Representative images with semi-quantitative analysis of survivin positive cells in myocardium in groups that were challenged with LPS or either pretreated with simvastatin 20 or simvastatin 40 before LPS. Immunohistological staining of myocardial tissues was performed using a p65-specific antibody to evaluate NF-κB p65 expression in cardiomyocytes, magnification 200x and 400x. (a) Control group. Note subsets of cardiomyocytes positive for NF-κB/p65 in the cell cytoplasm and/or nucleus in the LPS group (b), and intensive nuclear immunostaining in the simvastatin 20 (c) and simvastatin 40 (d) groups. (e) Semiquantitative analysis of NF-κB/p65 expression. *p < 0.01 in comparation with LPS group, ^#p < 0.05 in comparation with simvastatin 20 group. (f) The correlations of survivin expression and NF-κB/p65 positive cardiomyocytes within the experimental groups (fa, fb, fc).