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. 2019 Dec 27;9:20183. doi: 10.1038/s41598-019-56366-2

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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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Endothelin pathway markers in HSC. Bar diagrams show protein quantification of (A) P-moesin, (B) P-ERK1/2 (C) cFOS (D) αSMA (E) ETRA and (F) ETRB in HSC from control diet (CD-Veh, n = 5), and high-fat glucose-fructose diet rats treated with vehicle (HFGFD-Veh, n = 5), simvastatin (HFGFD-Sim, n = 5) or atorvastatin (HFGFD-Ato, n = 5). Full-length gels are included in Supplementary Fig. 5. GAPDH was used as loading control. Protein levels are normalized to HFGFD-Veh group and expressed as mean ± SEM. **p < 0.01 compared to CD-Veh; ^#p < 0.05, ^##p < 0.01 compared to HFGFD-Veh (ANOVA).