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. 2014 May 13;12(5):2922–2936. doi: 10.3390/md12052922

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© 2014 by the authors; licensee MDPI, Basel, Switzerland.

This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).

PMC Copyright notice

Ech A protected mitochondrial functions against cardiotoxic agent-induced damage. H9c2 cells were treated with cardiotoxic agents for 1 h cellular and mitochondrial oxygen consumption rate (OCR) and coupling efficiency was measured using an XF24 analyzer, respectively. (A) Cardiotoxic agents inhibited cellular OCR, but co-treatment with Ech A prevented this inhibition. (B) Cardiotoxic agents inhibited mitochondrial OCR, but co-treatment with Ech A prevented this inhibition. (C) Moreover, Cardiotoxic agents also inhibited coupling efficiency, but co-treatment with Ech A prevented this inhibition. Four independent in vitro experiments were performed. P < 0.05 vs. cardiotoxic agent single treatment group.