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. 2020 Jun 5;20:269. doi: 10.1186/s12872-020-01492-3

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 2 — Extractive β1AA decreased the rate of survival and increased the rate of apoptosis in myocardial H9C2 cells. a The results of CCK8 assay. β1AA significantly inhibited the cell proliferation. The effect of β1AA could be mimiced by isoprenaline, an agonist of β1AR and be inhibited by atenolol, an antagonist of β1AR. b The results of LDH assay. β1AA significantly increased the apoptosis of H9C2 cells. This effect could also be mimicked by isoprenaline and inhibited by atenolol. c TUNEL positive nuclei obtained from H9C2 cells visualized by fluorescence microscopy. Scale bar, 100 μm. d Group data of apoptosis rate of TUNEL assay (n = 5). E and F. β1AA significantly inreased the mRNA and protein expression of the β1AR (n = 5). The effects of β1AA on β1AR could be inhibited by atenolol. **, P ≤ 0.01. Group data presented by mean ± SEM