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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) treatment inhibited hepatobiliary fibrosis in mice. DIZE reduced the activation of hepatic stellate cells, as reflected by a reduced expression of α-smooth muscle actin (α-SMA) (A,E) and extracellular matrix protein, collagen 1 (B) leading to a marked reduction in biliary fibrosis (C,D) in both BDL and Mdr2-KO mice. Positive brown color staining for liver α-SMA by immunohistochemistry (arrows in panel E) and picrosirius red staining of bridging fibrosis (arrows in panel C) and fibrosis around portal triads (arrow heads in panel C) are shown (×200). Each bar represents the mean ± SEM profile from 10–15 mice per treatment group.