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. 2019 Mar 6;9:3633. doi: 10.1038/s41598-019-40002-0

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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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The effects of lithocholic acid (LCA) on hypertrophy are mainly mediated through protein kinase A (PKA) in H9c2 cells. (A) The effects of LCA were reversed by PKAI at the indicated doses; the right side shows the morphological changes in H9c2 cells, and the left side indicates the quantified data. (B) The effects of LCA treatment were also reversed by H-89 at the indicated doses; the right side shows the morphological changes in H9c2 cells, and the left side indicated the quantified data as described above. (C) Effects of LCA were not modified by ESI-09 treatment at doses effective to inhibit Epac; the right side shows the morphological changes in H9c2 cells, and the left side indicates the quantified data as above. Therefore, the LCA-induced alleviation of hypertrophy induced by high glucose is mainly mediated through the PKA pathway (*p-value < 0.05, **p-value < 0.01 versus control group; ^#p-value < 0.05, ^##p-value < 0.01 versus vehicle group, n = 6).