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. 2018 Jul 5;8:10175. doi: 10.1038/s41598-018-28490-y

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© The Author(s) 2018

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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Diminazene aceturate (DIZE) had no effect on angiotensin converting enzyme 2 (ACE2) activity and on other RAS components. DIZE did not change the expression of ACE2 gene (A) or ACE2 protein activity (B) in BDL or Mdr2-KO mice. This was further confirmed by hepatic levels of angiotensin II (Ang II) (C) and angiotensin-(1-7) (Ang-(1-7)) (D) peptides which were not different between DIZE and saline treated BDL or Mdr2-KO mice. DIZE treatment in BDL and Mdr2-KO mice failed to affect gene expression of the RAS components such as angiotensin converting enzyme (ACE) (E), angiotensin II type 1 receptor (AT1-R) (F) and Mas receptor (Mas-R) (G) in the liver. Each bar represents the mean ± SEM profile from 10–15 mice per treatment group.