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. 2017 Jul 13;7:5279. doi: 10.1038/s41598-017-05433-7

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© The Author(s) 2017

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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ELV-N32 and ELV-N34 enhance abundance of pro-homeostatic proteins and decrease abundance of cell damaging proteins in RPE cells under UOS. ELV-N32 or ELV-N34 indicates the sodium salt forms, and ELV-N34-Me or ELV-N32-Me indicates the methyl ester forms. ELVs induces the following effects in ARPE-19 cells undergoing UOS: (a) Concentration-dependent (100 and 250 nM) upregulation of SIRT1. The results are the averages of three independent experiments; (b) upregulation of Iduna abundance; (c) increased abundance of anti-apoptotic proteins Bcl-2 and Bcl-xL; (d) decreased abundance of pro-apoptotic proteins Bax, (e) Bid and (f) Bim. (g) Concentration-dependent (100 and 250 nM) upregulation of Prohibitin (type-1) by ELVs takes place. (h) Concentration-dependent (50, 100, 250, and 500 nM) reduction of UOS-induced apoptosis. Error bars, SEM; *p < 0.05. Also, see Supplementary Figs 4 and 5.