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. 2017 Jun 20;7:3909. doi: 10.1038/s41598-017-04018-8

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© The Author(s) 2017

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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Impairment of TLR4 attenuates the activation of HSCs in the PABF caused by Clonorchis sinensis. Livers from TLR4 wild and mutated mice infected with or without C. sinensis were harvested, and the sections of tissue containing bile ducts were fixed by 4% formalin solution for IHC. The activation of HSCs was indicated by immunohistochemical staining of α-SMA. (A) Representative images of α-SMA staining on HSCs of TLR4 wild or mutated mice as indicated. Scale bars for upper panel are 50 μm and for the nether panel are 10 μm, respectively. (B) The expression of α-SMA were semi-quantitated by independent pathologists as described in Methods and Materials. The data were obtained from 3~5 mice of three-independent experiment. The values were expressed as mean ± SEM. Compared with indicated mice, *P < 0.05, **P < 0.01, ***P < 0.001.