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. 2017 Aug 29;7:9793. doi: 10.1038/s41598-017-09470-0

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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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Serelaxin improved heart function of DOCA-salt rats. (a–f) Markers of cardiac hypertrophy and dysfunction as determined by quantitative real-time PCR (qRT-PCR) analysis of α-MHC, β-MHC, BNP, ANF, SERCA in the heart of DOCA-salt rats. Treatment with serelaxin increased α-MHC/β-MHC, decreased BNP and ANF, and increased SERCA. (g) Cardiac fibrosis determined by Picro Sirius Red staining for fibrillary collagens. DOCA induced cardiac fibrosis and treatment with serelaxin prevented the cardiac fibrosis. (h) Cardiac fibrosis as determined by Second Harmonic Generation (SHG) Microscopy showed DOCA induced a marked increase in cardiac fibrosis and that treatment with serelaxin markedly decreased the cardiac fibrosis. Results are expressed as means ± SEM (n = 6 rats). Statistical analysis was performed with one-way ANOVA.