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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 4. — Effect of AID‐TAT peptide on cellular superoxide in vitro. A, Representative traces of DHE recorded in a myocyte before and after 5 minutes exposure to 40 μmol/L of H₂O₂ followed by 5 minutes of exposure to 10 U/mL of catalase and a myocyte before and after 5 minutes of exposure to 0 μmol/L of H₂O₂ followed by 5 minutes of exposure to 10 U/mL of catalase. Vertical arrows indicate when drugs were added. B, Mean±SEM of changes in DHE for all myocytes exposed to 40 μmol/L of H₂O₂, 10 U/mL of catalase, and 10 μmol/L of nisoldipine (Nisol) as indicated. Inset above: the superoxide scavenger, N‐tert‐butyl‐α‐phenyl‐nitrone (PBN), caused a 93.6±1.9% decrease in the rate of DHE signal. C, Representative traces of DHE recorded in myocytes before and after 5 minutes of exposure to 40 μmol/L of H₂O₂ followed by 5 minutes of exposure to 10 U/mL of catalase in the presence of either 1 or 10 μmol/L of AID(S)‐TAT or AID‐TAT peptide as indicated. Vertical arrow indicates when drugs were added. D, Mean±SEM of changes in DHE for all myocytes exposed to 40 μmol/L of H₂O₂, 10 U/mL of catalase, 1 or 10 μmol/L of AID(S)‐TAT or AID‐TAT peptide, and 10 μmol/L of nisoldipine (Nisol) as indicated. Inset above: Mean±SEM of changes in DHE for myocytes before and 30 and 60 minutes after exposure to 10 μmol/L of AID‐TAT peptide as indicated. Statistical significance was determined using the Kruskal‐Wallis test followed by Dunn's multiple comparison test. AID indicates alpha‐interacting domain; DHE, dihydroethidium; TAT, transactivator of transcription.