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. 2016 May 17;7:124. doi: 10.3389/fphar.2016.00124

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Copyright © 2016 Samokhvalov, Jamieson, Fedotov, Endo and Seubert.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Inhibition of SIRT1 activity abolished 19,20-EDP protective effects against H/R induced cytotoxicity. HL-1 cardiac cells were subjected to either 30 h normoxia or 24 h hypoxia and 6 h reoxygenation in the presence of 19,20-EDP (1 μM) and EX-527 (1 μM) for 24 h. Inhibition of SIRT1 activity blocked DHA and EDP protective effects toward (A) cell viability and (B) mitochondrial activity as assessed by MTT assay. (C) The relative rates of increased mitobiogenesis triggered by EDPs were attenuated by inhibition of SIRT1 activity. (D) EDPs limited HIF-1α DNA-binding activity caused by H/R injury, which were blocked by inhibiting SIRT1 activity. Values are represented as mean ± SEM; N = 3 independent experiments; ^∗p < 0.05 treatment vs. normoxic control, ^#p < 0.05 treatment group vs. H/R control or DHA/MSPPOH.