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. 2017 Apr 6;7:693. doi: 10.1038/s41598-017-00782-9

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© The Author(s) 2017

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Role of TLR4 in the activation of MAPKs and NF-κB pathways by SAA1 in human amnion fibroblasts. Effect of TLR4 inhibitor CLI095 (5 μM) on the increases in the phosphorylation of p38 (A, n = 5), ERK1/2 MAPKs (B, n = 4) and p65 (C, n = 4), and the decrease in IκBα (D, n = 4) abundance induced by SAA1 (10 ng/mL, 60 min) in human amnion fibroblasts. Top panels are the representative immunoblots. Data are the means ± SEM. Statistical analysis was performed with one-way ANOVA test. *P < 0.05, ***P < 0.001 vs. control (0), ^#P < 0.05, ^##P < 0.01, ^###P < 0.01 vs. SAA1.