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. 2018 Jun 22;8:9568. doi: 10.1038/s41598-018-27907-y

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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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GAL-1 regulates blood leukocyte recruitment. (A–D) Representative dot plots of leukocytes (each point represents a cell) immunostained for adhesion molecules CD62L (conjugated with PE) and CD11b (conjugated with FITC). Groups: (A) SHAM, (B) ischaemia-reperfusion (IR), (C) IR treated with dexamethasone (DEXA), or (D) GAL-1, 30 min before IR. (E–G) Percentage of CD62L⁺, CD11b⁺ or double labelled to CD62L⁺/CD11b⁺. The percentage of CD62L⁺/CD11b⁺leukocytes increased in the IR group. These alterations were reversed with DEXA or GAL-1 treatments. (F) There was no significant difference in CD62L⁺ and CD11b⁺ expression among the studied groups. Data represent the median ± SD of the percentage of cells. **p < 0.01, IR vs SHAM. ⁺⁺p < 0.01 and ⁺⁺⁺p < 0.001 vs IR, one-way ANOVA test, N = 6/group.