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. 2020 Feb 20;10:3054. doi: 10.1038/s41598-020-59888-2

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© The Author(s) 2020

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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Schematics showing the potential mechanisms underlying the protective effects of P188. Blunt force trauma increases ROS. The oxidative stress-sensitive signaling pathways (e.g., NF-kB) can up-regulate MMP- 2 & 9 in the brain endothelium which, in turn, degrades the tight junction structure and integrity. The brain endothelium transport properties are modulated and lead to an increased BBB permeability. The BBB protection by P188 against traumatic brain injury is proposed to be mediated by resealing the compromised cell membrane, decreasing the ROS levels, down-regulating MMPs, which inhibits the degradation of tight junction, and thereby restores the biotransport properties of the brain endothelium. Collectively, P188 attenuates the extent of injuries caused by blunt force brain traumas.