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. 2021 Aug 30;18:188. doi: 10.1186/s12974-021-02226-8

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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. 5 — Blockade of TAK1 prevents neuronal pyroptosis through activating NLRP3 inflammasome. a Representative immunoblot images and b quantification of NLRP3, ASC, cleaved caspase-1, IL-β, and IL-18 in the ipsilateral cortex 24 h after SAH. c Western blotting and d quantitative analysis of NLRP3, ASC, cleaved caspase-1, IL-β, and IL-18 in Ctrl-, OxyHb-, and OxyHb+OZ-treated neurons. Data are expressed as mean ± SD, n = 5 per group. ***P < 0.001 vs Sham group; ^##P < 0.01, ^###P < 0.001 vs SAH+Vehicle group. ^†††P < 0.001 vs Control group;^§§§P < 0.001 vs OxyHb group