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. 2017 Jun 27;7:4299. doi: 10.1038/s41598-017-04082-0

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© The Author(s) 2017

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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Cilostazol significantly suppressed endothelial adhesion molecule expression in the corpus callosum. (a) Representative images of intercellular adhesion molecule-1 (ICAM1) staining in the corpus callosum. (b) There was a significant difference in ICAM staining between the three groups (F _{(2, 33)} = 13.19; p < 0.0001). ICAM1 immunostaining was significantly greater in the hypoperfused-control group compared to the sham (p < 0.001) and this was reduced with cilostazol treatment (p < 0.01). (c) There was a significant association between ICAM1 positive areas and microgliosis (Pearson r = 0.375, p < 0.05), and the number of revisiting errors (Pearson r = 0.412, p < 0.05). Data represents mean ± SEM.