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. 2018 Dec 24;8:18062. doi: 10.1038/s41598-018-36138-0

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© The Author(s) 2018

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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MLC901 reduced the increase in CNS-associated phagocytes induced by focal 60-min ischemia in mouse brains. (A) Representative bivariate dot plots of Percoll isolated brain cells illustrating on the identification of microglia (CD11b⁺/CD45^low+), CNS-associated phagocytes (CD11b⁺/CD45^high+) and immune cells (CD11b⁻/CD45^high+). (B) Histograms of average percentage of CNS- associated phagocytes (left) and microglia (right) in live single immune cells from reperfused (R) or not reperfused (NR) brains of mice submitted to 60-min focal ischemia and treated with vehicle (black bars) or MLC901 (ip injection, 40 μg/kg) (n = 6 to 10 per experimental group) and sacrificed 24 hours after MCAO. Data are reported as mean ± SEM. **P < 0.01, ***P < 0.001 versus sham-operated group and ^$$P < 0.01, ^$$$P < 0.001 versus vehicle ischemic group, #P < 0.05 versus non-reperfused MLC901-group (Kruskal-Wallis test, H_(4,54) = 35.39).