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. 2018 Aug 23;8:12708. doi: 10.1038/s41598-018-31137-7

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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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SFN modulate the redox-metabolic interplay of the brain vascular endothelium to promote ATP production. SFN promotes upregulation of Glut1 expression (A) and transport activity (B) as determined by 2-NBDG uptake normalized to total protein. (C) Key genes involved in the regulation of glycolysis were also upregulated including hexokinase 1 (Ht1) and pyruvate kinase 2 (Pkm2) as analyzed by MitoChip array (C1) and confirmed by RT-PCR (C2). The overall cellular effect was a substantial increase in ATP production (D). N = 3 independent biological samples per condition assayed in triplicates. “*”p < 0.05, “**”p < 0.01 compared to controls (fold changes). For the time-dependent study (24 vs. 48 h SFN treatment) “+” p < 0.05 vs. 24 h. Blots of Glut1 and β-actin were taken from different gels.