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. 2020 Sep 17;10:15316. doi: 10.1038/s41598-020-72136-x

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© The Author(s) 2020

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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Activation of STAT3 in mouse tissues following CLP-induced sepsis. (A) Time course of changes in STAT3 phosphorylation in lung, liver, kidney, and heart tissues after CLP. Representative Western blots of phospho-STAT3 at Tyr-705 and of total STAT3 are shown. (B) The summarizing data obtained in lung, liver, and heart tissues are presented as phospho-STAT3/STAT3 expressed relative to the respective control (sham-operated) (n = 8). (C) Time course of phosphorylation levels of JAK2 at Tyr-1007 and Tyr-1008 in liver tissues were quantified by Western blot analysis (n = 8). (D) Time course of phosphorylation levels of Src at Tyr-416 in liver tissues were quantified by Western blot analysis (n = 8). Typical Western blots are shown in the left side and the summary of quantification of densitometric measurement as a ratio of phosphorylated molecule relative to total expression is presented in the right side of each panel. GAPDH served as loading control. *P < 0.05, **P < 0.01, and ***P < 0.001 compared with sham-operated control (0 h).