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. 2018 Sep 4;17:123. doi: 10.1186/s12933-018-0767-z

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© The Author(s) 2018

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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.

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Fig. 5 — MiR-21 attenuates diabetic condition-induced cardiomyocyte hypertrophy in vitro. a Relative expression of miR-21 in treated H9c2 cells. b Representative images and relative cell area determined by quantitation analysis of cardiomyocyte by Phalloidin staining in treated H9c2 cells. c–e Relative expression levels of ANP, BNP, and β-MHC/α-MHC in treated H9c2 cells. f ROS generation in treated H9c2 cells. g Relative NO levels in treated H9c2 cells. h Protein levels of p-Akt(Ser473) and p-eNOS(Ser 1177) in treated H9c2 cells