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. 2018 May 1;8:6801. doi: 10.1038/s41598-018-25068-6

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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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AKAP-12, mitochondrial function and oxidative stress markers in hearts from Aldosterone-salt-treated rats. AKAP-12 immunostaining and protein expression (A,B) in myocardium from Controls, Aldo-salt-treated rats and Aldo-salt + Spiro-treated rats. Total mtDNA expression was measured (C). TAC and peroxide production (D). Oxidative stress markers (E). PGC-1α and PHB expressions (F). PGC-1α immunostaining (G). Magnification of the microphotographs 40x. Histogram bars represent the mean ± SEM of each group of subjects. For Western blot experiments, the blots were cropped, protein densitometry was expressed in arbitrary units (AU) once normalized to β-actin. *p < 0.05 vs Control; ^$p < 0.05 vs Aldo. AKAP-12, A-kinase anchoring protein 12; Aldo, Aldosterone; Spiro, Spironolactone; Total mtDNA, Total mitochondrial DNA; TAC, Total antioxidant capacity; CML, carboxy-methyl-lysine; MDA, malondialdehyde; PGC-1α, peroxisome proliferator-activated receptor-gamma coactivator 1 alpha; PHB, prohibitin.