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. 2022 Jun 11;19:141. doi: 10.1186/s12974-022-02501-2

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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. 9 — ITBS modulated microglial phenotypes via inhibiting TLR4/NFκB/NLRP3 signaling pathway. Immunofluorescence staining for Iba1 (A) and quantitative analysis (B) showed microglial activation over a time course from D1 to D7 after cerebral I/R injury (n = 4). Scale bar = 60 μm. Representative bands of the western blot (C, J) and quantitative analysis of Iba1 (D), CD86 (E), CD206 (F), iNOS (G), Arg1 (H), TLR4 (K), NFκB (L), p-NFκB (M) and NLRP3 (N) normalized to β-actin (n = 6). ITBS reduced protein levels associated with classical M1 phenotypic activation (CD86, iNOS) and elevated protein levels associated with alternative M2 phenotypic activation (CD206, Arg1), respectively. I KEGG pathway analysis of differentially expressed genes showed that the potential mechanism of iTBS regulating innate immune responses were highly associated with NOD-like receptor, Toll-like receptor and NFκB signaling pathways involved. ITBS also ameliorated the high levels of TLR4, NFκB, p-NFκB and NLRP3 reduced by cerebral ischemia. Values are expressed as the mean ± SEM of the mean. *P < 0.05, **P < 0.01 as determined by one-way ANOVA (Tukey's multiple comparison test)