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. 2019 Sep 6;20:351. doi: 10.1186/s12882-019-1534-4

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© The Author(s). 2019

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. 7 — Spironolactone (SPL) improves endothelial dysfunction in advanced glycation end products (AGEs) –stimulated human aortic endothelial cells (HAECs) through sirtuin-3 (SIRT3) protein mediation. (a) Downregulation of SIRT3 was noted in AGEs-stimulated HAECs. The addition of SPL at concentrations of 1 μM and 10 μM improved the SIRT3 protein expression. (b) SPL increased phospho-endothelial nitric oxide synthase (p-eNOS) activation at a concentration of 10 μM in AGEs-stimulated HAECs. However, pretreatment of AGEs-stimulated HAECs with tenovin-6 at a concentration of 1 μM abrogated the effect of SPL on the p-eNOS activation. * any groups compared with the vehicle, p < 0.05; # any groups compared with the AGEs group, p < 0.05