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. 2014 Jun 23;3(3):e000961. doi: 10.1161/JAHA.114.000961

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© 2014 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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Figure 1. — AID‐TAT peptide decreases ischemia‐reperfusion (I/R) injury in hearts ex vivo. A, Representative sections from guinea pig hearts after I/R treated with 1 μmol/L of scrambled (AID(S)‐TAT) or active (AID‐TAT) peptides. Infarct size is assessed as area that did not take up nitroblue tetrazolium dye. B, Mean±SEM of infarct size expressed as percentage (%) of total left ventricular (LV) area for all hearts treated with AID(S)‐TAT or AID‐TAT as indicated. C, Creatine kinase (CK) activity of hearts treated with 1 μmol/L of scrambled (AID(S)‐TAT) or active (AID‐TAT) peptides before (Pre) and after (Post) ischemia as indicated. D, Lactate dehydrogenase (LDH) activity of hearts treated with 1 μmol/L of scrambled (AID(S)‐TAT) or active (AID‐TAT) peptides before (Pre) and after (Post) ischemia as indicated. E, GSH/GSSG ratio of hearts treated with 1 or 10 μmol/L of scrambled (AID(S)‐TAT) or active (AID‐TAT) peptides before (Pre) and after (Post) ischemia as indicated. n represents number of hearts. Statistical significance was determined using the Kruskal‐Wallis test followed by Dunn's multiple comparison test. AID indicates alpha‐interacting domain; GSH/GSSG, glutathione to oxidized glutathione; TAT, transactivator of transcription.