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. 2021 Nov 5;18:255. doi: 10.1186/s12974-021-02306-9

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© The Author(s) 2021

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 — Carnosine treatment attenuates disease burden, acrolein-protein adduct formation and markers of neuroinflammation in EAE. a Clinical EAE disease severity, scored daily (day 0–56 post immunization) by a blinded assessor, indicates a significantly lower cumulative disease burden in animals receiving 3% carnosine compared to all other groups. n = 16 animals/group. b Detection of acrolein-protein adducts by western blot in healthy controls (dashed line), untreated EAE animals (0%) and following treatment with carnosine (3% in drinking water) in EAE. Groups receiving 0.3% and 1.5% were omitted to facilitate direct comparison of 0% and 3% carnosine on a limited number of blots. All treatment groups were compared in a preliminary experiment (data not shown). c, d Immunohistochemistry-based quantification of spinal cord T cell numbers (CD3) shows a reduction in carnosine-treated mice (3%) compared to untreated mice (0%) and mice treated with 0.3% or 1.5% carnosine in the drinking water. e, f Immunohistochemistry-based quantification of spinal cord microglia/macrophage numbers (F4/80) shows a reduction in carnosine-treated mice (3%) compared to untreated mice (0%). g, h Immunohistochemistry-based quantification of spinal cord reactive astrocyte area (GFAP) showed no treatment effect of carnosine. For figures d, f and h, all EAE groups exhibited a significant increase compared to healthy controls (statistics not shown). Figures d, f, h: n = 5–6 animals/group. i Spinal cord mRNA expression in healthy controls, untreated EAE animals (0%) and following treatment with different doses of carnosine (0.3%, 1.5%, 3% in the drinking water) in EAE. n = 5–6 animals/group. For all genes, untreated EAE groups (0%) exhibited a significant increase compared to controls (statistics not shown). Data are mean ± SD. One-way ANOVA or Kruskal–Wallis, post hoc testing *p < 0.05, **p < 0.01 between the indicated groups (a, d, f, h, i). Independent samples t-test *p < 0.05, control line is for reference (b). Scale bars are 100 µm (c, e, g)