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. 2021 Jun 28;11:13380. doi: 10.1038/s41598-021-92790-z

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© The Author(s) 2021

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Liver fibrosis and activationoh hepatic stellate cells (HSCs) in nonalcoholic steatohepatitis (NASH) rats. (A) Representative images of liver sections stained with hematoxylin and eosin (H&E), Sirius Red stain, and anti-α-SMA antibody. (B) The mRNA levels of liver fibrosis markers, transforming growth factor-β (Tgfb), collagen 1a1 (Col1a1), α-smooth muscle actin (Acta2), tissue inhibitor of metalloproteinase 1 (Timp1), and plasminogen activator inhibitor 1 (Serpine1). N = 5 per group. Statistical analysis among the three groups was performed using Kruskal–Wallis ANOVA. Only when a significant difference was found, Tukey's multiple comparison test was performed. *P < 0.05, **P < 0.01.