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. 2017 Oct 18;7:13424. doi: 10.1038/s41598-017-13949-1

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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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Proposed mechanism of BBG-mediated regulation of endothelial tolerance to ischemia-reperfusion injury The proposed mechanism of BBG-mediate regulation of endothelial tolerance to oxidative stress following ischemia-reperfusion injury through upregulation of VEGF and Parkin. BBG: barley-derived (1.3) β-D-Glucan; HDAC: class I histone deacetylase; Ac: acetyl; VEGF: vascular endothelial growth factor; VEGFR1: vascular endothelial growth factor receptor type 1; HIF-1α: hypoxia-inducible factor 1-alpha; MnSOD: manganese superoxide dismutase; O₂−: anion superoxide.