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. 2019 Apr 23;9:6354. doi: 10.1038/s41598-019-42936-x

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© The Author(s) 2019

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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AS-1 attenuates Ang II-induced hypertrophic response of cardiomyocytes by inhibition of ERK1/2 phosphorylation in vitro. Rat primary cardiomyocytes were stimulated with Ang II (0.1 μM) for 24 hours. AS-1 (100 μM) or DMSO was administrated 30 minutes before Ang II induction. (A–C) The mRNA expression of ANP (A), BNP (B) and β-MHC (C) in primary cardiomyocytes was measured in each group. (D) Representative images of primary cardiomyocytes stained with anti-actinin, a marker for α-cardiac muscle actinin, by immunofluorescence. (E) Representative images of total ERK1/2 and phosphor-ERK1/2 protein levels in primary cardiomyocytes by western blot. con: non-treated cells. Ang II: cells induced by Ang II. Ang II + DMSO: cells administrated with DMSO followed by Ang II induction. Ang II + AS-1: cells administrated with AS-1 followed by Ang II induction. Mean ± SEM, n = 4, *p < 0.05, **p < 0.01.