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. 2021 Dec 4;7:374. doi: 10.1038/s41420-021-00768-7

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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 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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Fig. 4 — A The expression levels of BECN1, p62, LC3B, vimentin, and α-SMA were detected by western blot in TAA-induced mouse liver fibrosis. B Double IF staining of α-SMA and LC3B. C Western blot revealed that BBR inhibited autophagy in HSC-LX2. D, E Costaining of α-SMA and Atg5 or Atg7. F, G HSC-LX2 cells were treated with or without BBR (21 μM) for 24 h; protein expression of Atg5, Atg7, α-SMA, LC3B, and p62 and the relative mRNA levels of Atg5, Atg7, COL1A1, and α-SMA were assayed by western blot and qPCR. H HSC-LX2 cells were treated with or without BBR (21 μM) for 24 h; transmission electron microscopy ultrastructural features of autophagosomes are presented. The results are expressed as mean ± SD. Data are representative of three independent experiments; n = 3–6 in every group; Scales: 1 or 100 μm. Representative photographs are shown. Compared with the control group, *P < 0.05, **P < 0.01; compared with the model group, ^##P < 0.01. NS, not significant.