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. 2019 Dec 13;16:264. doi: 10.1186/s12974-019-1665-3

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. 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.

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Fig. 4 — EA treatment attenuates neuroinflammation and decreases the expression levels of oxidation-related proteins in 5XFAD mice. a Representative blots for the expression of neuroinflammatory proteins (CD11b, GFAP, and COX2) from non-Tg, Tg, and EA-treated Tg (Tg + KI3) mice. Tubulin was used as the loading control. b Quantification of the CD11b, GFAP, and COX2 expression levels (n = 3–4/group). c Representative immunoreactive bands showing the expression of oxidation-related proteins (HO-1, transferrin, and Bax) in the prefrontal cortex. Tubulin was used as the loading control. d Quantification of the HO-1, transferrin, and Bax expression levels (n = 3–4/group). Data are presented as means ± SEM (*p < 0.05, **p < 0.01, ***p < 0.001)