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. 2021 Jan 7;12:15. doi: 10.1186/s13287-020-02070-2

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© The Author(s) 2021

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. 2 — MSC-derived PGE₂ restrains inflammatory responses in the liver during LPS/D-Gal-induced ALF. a The mRNA levels of pro-inflammatory cytokines (IL-1β, CCL2, iNOS, TNF-α) in the liver in each group (n = 4). b The protein expression levels of NF-κB signaling in each group. c The protein expression levels of TAK1 signaling in each group. d Serum levels of ALT and AST in mice pretreated with TAK1 inhibitor, 5Z-7-ox (n = 4). e Representative HE-stained liver sections and quantitation of necrosis area in each group (n = 4). f Protein levels of TAK1 and NF-κB signaling in each group (*p < 0.05, **p < 0.01, ***p < 0.001)