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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 decreased microglial activation and neutrophil recruitment in the reperfused brain 24 hours following MCAO. (A–D) Representative immunohistochemical staining for Iba1 microglia marker (A) myeloperoxidase (MPO) (B) and GFAP astrocytic marker (C) in brains of vehicle- and MLC901-treated mice 24 hours after MCAO. (A) Representative views of Iba1 immunopositive cells in ischemic penumbra, ischemic core and contralateral control side of vehicle- and MLC901-treated mice. Diagram boxes indicate the regions where the images in middle and bottom panels at higher magnification were acquired (B,C) Representative immunostaining of MPO (B) and GFAP (C) in ischemic penumbra of vehicle- and MLC901-treated mice. (D) Quantitation of Iba1 expression (AU positive microglia pixel intensity) in ischemic penumbra and ischemic core of vehicle- and MLC901-treated mice. Scale bar, 20 μm (top panels), 50 μm (middle and bottom panels) (n = 6 per experimental group).