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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 attenuated cardiotoxic agent-induced mitochondrial damage in H9c2 cells. Cells were treated with cardiotoxic agents for 1 h, after which ROS level and mitochondrial membrane potential were measured using a microplate assay. (A) Cardiotoxic agents rapidly increased ROS (CM-H₂DCFDA) level and (B) decreased mitochondrial membrane potential (ΔΨm, TMRE). Co-treatment with Ech A attenuated the increase in reactive oxygen species (ROS) level and preserved mitochondrial membrane potential. Four independent in vitro experiments were performed. P < 0.05 vs. cardiotoxic agent single treatment group.