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. 2018 Aug 22;8:12552. doi: 10.1038/s41598-018-30675-4

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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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Cerebral hypoperfusion induces pro-inflammatory gene expression in the optic tract and Nrf2-overexpression reduces the expression of complement component 4. (a) Nrf2 and (b) Gclm expression in the optic tract was significantly higher in GFAP-Nrf2 animals (F_(1,32) = 116.4, p < 0.0001, F_(1,31) = 49.83, p < 0.0001 respectively), but was not altered by hypoperfusion. (c) C4 expression in the optic tract was significantly increased by hypoperfusion (F_(1,32) = 8.07, p = 0.008) with a significant effect of genotype (F_(1,32) = 5.66, p = 0.02). (d) Hypoperfusion significantly increased C1q and (e) Ccl3 expression in the optic tract (F_(1,32) = 7.92, p = 0.008, F_(1,29) = 8.68, p = 0.006; respectively), but reduced the expression of Ccl2 (F_(1,31) = 6.09, p = 0.02). There was no effect of genotype on the expression of C1q, Ccl3 or Ccl2. Gene expression was normalised to Gapdh or 18S and expressed relative to WT sham controls. Dashed line indicates average WT sham level. Mean ± SEM. Two-way ANOVA with Bonferroni adjustment for post hoc analysis. *p < 0.05, **p < 0.01, n = 8–10 per group.