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. 2017 Nov 17;7:15797. doi: 10.1038/s41598-017-16124-8

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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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Effects of MyD88 inhibition on p-TAK1, IκBα, and p65 expression 24 h post SAH. Western blots show TAK1, p-TAK1 (a), IκBα (b) and p65 (c) levels following SAH. The upper panel shows representative protein levels of TAK1, p-TAK1, IκBα, and p65. The bottom panels are quantitative data of p-TAK1, IκBα, and p65. Tubulin and histone-3 were used as loading controls. Data are expressed as mean ± SD (n = 6 in each group). p-TAK1, phosphorylated transforming growth factor-β-activated kinase 1, IκBα, inhibitor of NF-κB, Definition of SAH is the same as in Fig. 2. *p < 0.05 compared with the sham group, ***p < 0.001 compared with the sham group, ^#p < 0.05 compared with the SAH group, ^##p < 0.01 compared with the SAH group, ^###p < 0.001 compared with the SAH group, NS, no statistic difference compared with the SAH group.