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. 2017 Sep 7;8(9):e3044. doi: 10.1038/cddis.2017.439

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Copyright © 2017 The Author(s)

Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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Nuclear AT1 and AT2 receptors in aged rats and mice. Nuclei isolated from brains of aged rats showed a significant decrease in the levels of both AT1 and AT2 receptors (a). Treatment of nuclei with AII did not induce any significant increase in AT2, angiotensinogen (ANG) and PGC-1α mRNA expression (b), or in the levels of nuclear superoxide/H₂O₂ (c). Levels of nuclear superoxide/H₂O₂ were significantly lower in aged KO AT1 mice than in WT aged mice, and treatment with AII did not induce any significant increase in superoxide/H₂O₂ in nuclei from aged KO AT1 mice (d). Data are mean±S.E.M. *P<0.05 compared to the corresponding control, ^#P<0.05 compared to aged WT or aged WT treated with AII. One-way analysis of variance and Holm–Sidak post hoc test (b and d) and Student’s t-test (a and c) (n=3–8)