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. 2022 Nov 12;13:516. doi: 10.1186/s13287-022-03196-1

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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. 6 — EMS combined with EPC treatment protects the rat brain against BICAL-induced Tau phosphorylation. Representative immunoblot (left) and quantification (right) of A pGSK3β (Y216) and B pTau (Ser199) in the control, BICAL, and treatment group rats. EMS combined with EPC treatment significantly decreased the pGSK3β/GSK3β and pTau/Tau ratios as compared with the BICAL group. C Representative microphotography showing immunoexpression of pTau (Thr231) (shown in brown) in the cerebral cortex, hippocampus CA1, and dentate gyrus (DG) regions of the control, BICAL, and EMS combined with EPC treatment rats. *p < 0.05, **p < 0.01, ***p < 0.001, n = 4–6. Scale bars = 100 µm (upper panel) and 50 µm (lower panel)