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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. 7 — MSC-derived PGE₂ protects against liver inflammation via EP4. a The mRNA levels of inflammatory cytokines (IL-1β, CCL2, iNOS, TNF-α) in the liver from each group pretreated with EP4 inhibitor (EP4i) (n = 4). b The protein expression levels of NF-κB signaling in each group pretreated with EP4i. c The protein expression levels of TAK1 signaling in each group pretreated with EP4i. d The protein expression levels of NLRP3 inflammasome signaling in each group pretreated with EP4i. e Measurement of caspase-1 enzymatic activity in the liver of each group pretreated with EP4i (n = 4). f Protein levels of NLRP3 inflammasome and TAK1 signaling in BMDM pretreated with EP4i or knocking down of EP4 via siRNA. g The levels of IL-1β in supernatants of BMDM pretreated with EP4i or knocking down of EP4 via siRNA (*p < 0.05, **p < 0.01)