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. 2022 Jun 11;19:143. doi: 10.1186/s12974-022-02512-z

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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. 5 — Treg inhibited pro-inflammatory factors via microglial activation in the brain of TMT-intoxicated. The expression of Iba1 was observed in the hippocampi of TMT-intoxicated mice using immunostaining (A). The number of Iba1-positive cells in CA1 and CA3 (B) was measured (n = 10–13 mice/group). The protein levels of pro-inflammatory cytokines, including TNFα, IL-1β, and IL-6, in the brain were measured using ELISA and calculated as a relative for Con (C) (n = 3–5 mice/group). The relative mRNA levels of pro-inflammatory microglia-associated markers, including TNFα, NOS2, IL-1β, and IL-6, and anti-inflammatory markers, TGFβ, Mrc1, Arg1, and BDNF in the brain were analyzed (D) (n = 3–5 mice/group). Data are presented as the mean ± SEM. Significance was determined by Tukey’s HSD (*p < 0.05, **p < 0.01 vs. the Con group and ^#p < 0.05, ^##p < 0.01, ^###p < 0.001 vs. the TMT group)