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. 2016 Apr 18;17:15. doi: 10.1186/s12868-016-0251-1

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© Cao et al. 2016

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 3 — Effects of GCPII KO on the expression of mitochondrial Bcl-2 and Bax. Representative immunoblots (a) and densitometric analysis (b) revealed a significant reduction in the mitochondrial Bcl-2/Bax ratio following TBI in both wild type and KO mice. The ratio in GCPII KO mice was significantly higher than their WT counterparts. The immunoblot data were scanned and normalized to the density of VDAC. The ratio of the normalized data for the wild type/sham mice was given a value of one. Data from other groups are expressed as values relative to the value for the wild type/sham mice. Data were represented as mean ± SEM (n = 6 per group); *p < 0.05, versus sham control of the same genotype; ^# p < 0.05, versus injured wild-type mice