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. 2020 Jan 2;44(1):411–422. doi: 10.1007/s10143-019-01228-8

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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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — Expression of the GLUT1, GLUT3, and HIF-1α proteins in the pericontusional cortex. Electrophoretic band photographs of the western blot analysis of GLUT1, GLUT3, HIF-1α, and β-actin proteins in the cortex. As shown in the graphs, TBI caused an increase in protein expression of GLUT1 (A), GLUT3 (B), and HIF-1α (C) compared with those in the sham group (n = 6 animals per group,*p < 0.05), and HPC increased the expressions of GLUT1 (A), GLUT3 (B), and HIF-1α (C) proteins after TBI. Data are expressed as means ± SD (n = 6 animals per group, ^#p < 0.05)