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. 2022 Apr 6;19:80. doi: 10.1186/s12974-022-02445-7

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© The Author(s) 2022

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. 1 — NLRP3 inflammasome is activated in neurons in SDH of IC rats, and MCC950 inhibits the NLRP3 inflammasome activation. A–E Western blot analysis showing that expression levels of NLRP3, Caspase-1, IL-1β and IL-18 were significantly increased in SDH of IC rats compared with normal rats, and MCC950 treatment significantly decreased expression levels of NLRP3, Caspase-1, IL-1β and IL-18 in SDH of IC rats. n = 8 per group. *P < 0.05. F Immunofluorescence co-staining showing that NLRP3 was colocalized predominantly with NeuN (neuron marker), but scarcely with GFAP (astrocyte marker) or OX-42 (microglia marker) in the SDH. Scale bars = 200 μm