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. 2021 Mar 23;18:80. doi: 10.1186/s12974-021-02071-9

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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. 10 — Effects of ligature-induced periodontitis on STAT3 signaling pathway. Expression of pSTAT3 in periodontal tissue (a) and cortex (b) was detected via immunohistochemistry (×100 and ×400, bar = 200 μm and 50 μm, respectively). Expression of JAK2, STAT3, and pSTAT3 (Tyr-705) was further measured by WB (c–h). High expression of pSTAT3 was effectively inhibited by CTS. pSTAT3/STAT3 was upregulated by the periodontal ligature. The quantification of related protein expression: d JAK2 in periodontal tissue (F = 1.800, p = 0.2251), e pSTAT3 (Tyr-705)/STAT3 in periodontal tissue (F = 6.685, p = 0.0143), g JAK2 in cortex (F = 1.361, p = 0.3224), h pSTAT3 (Tyr-705)/STAT3 in the cortex (F = 6.169, p = 0.0178). (n = 3 per group, one-way ANOVA, *p < 0.05 compared to the control group and #p < 0.05 compared to the CP group)