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. 2023 Sep 11;20:208. doi: 10.1186/s12974-023-02879-7

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© The Author(s) 2023

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 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. 7 — H3K18la/NFκB signaling axis aggravate brain aging and Alzheimer's disease pathology by upregulating IL-6 and IL-8. A, B Immunoblotting results displaying changes in levels of p–p65 and p65 in BV2 (A) or HMC3 (B) cells treated with indicated. C, D Cell immunofluorescence results indicating the nuclear activation of p65 in BV2 (C) or HMC3 (D) cells treated with indicated, scale bar, 10 μm. E, F q-PCR detection of the expression levels of SASP components in BV2 (E) or HMC3 (F) cells treated with indicated. Data are presented as means ± SD from three biological experiments. Each bar represents the mean ± s.d. for triplicate experiments, *p < 0.05, **p < 0.01, ***p < 0.001, N.S.: no significance