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. 2017 Jun 19;7:3846. doi: 10.1038/s41598-017-03309-4

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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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CCI-TBI induces ROS free radical production in ipsilateral cortex area of injury. In vivo dihydroethidium staining detection in naive (A) vs. 4 hrs following CCI-TBI (B) cerebral cortex in area of CCI-TBI impact site (4X). Red fluorescence indicates oxidation of dihydroethidium and in situ ROS free radical detection. The impact site and affected ipsilateral cortical tissue is outlined with a white dotted line. ROS detection extends through and beyond the depth of the cortex. (C) Quantification of dihydroethidium fluorescence intensity in naive compared to CCI-TBI groups at 4 hrs post-injury. Data are presented as mean ± SD. (Two-tailed unpaired t test with equal SD P = 0.0002, t = 12.83, df = 4).