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. 2022 Nov 2;20:497. doi: 10.1186/s12967-022-03692-1

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© The Author(s) 2022

Open AccessThis 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/. 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 in a credit line to the data.

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Fig. 3 — Inhibition ofAnxa2improved hepatocyte pyroptosis and liver fibrosis in NASH mice. (A) WB for detecting the inhibitory effects from Lv-shAnxa2 on the expression of ANXA2 and pyroptosis related proteins (including ASC, pro-Caspase1, C-Caspase1, GSDMD, and GSDMD-N) in liver tissues of NASH mice. (B) HE staining for detecting the pathological changes of NASH liver. (C) Masson staining for detecting the effects of Anxa2 inhibition on liver fibrosis. (D) Immunohistochemical staining for detecting the effects from Anxa2 inhibition on α-SMA expression. (E) The serum levels of ALT, AST, IL-1β, and CRP. Eight mice were included in each group. *: P < 0.05; **: P < 0.01; ***: P < 0.001; ****: P < 0.0001