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. 2018 May 8;18:60. doi: 10.1186/s12876-018-0789-8

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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. 3 — Histological images using Picro-sirius red staining (a-c) of liver tissue for fibrosis and immunohistochemical staining for αSMA (d-f) in mice treated with 8 weeks of thioacetamide (TAA) with or without FXa or thrombin inhibition. Control mice treated with TAA (n = 13) alone (A; × 15magnification). Mice treated with TAA and the thrombin inhibitor (n = 12), Dabigatran (100 mg/kg) (B; × 15 magnification). Mice treated with TAA and the FXa inhibitor (n = 13), Rivaroxaban (40 mg/kg) (C; × 15 magnification)