Echinochrome a protects mitochondrial function in cardiomyocytes against cardiotoxic drugs

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Abstract

Echinochrome A (Ech A) is a naphthoquinoid pigment from sea urchins that possesses antioxidant, antimicrobial, anti-inflammatory and chelating abilities. Although Ech A is the active substance in the ophthalmic and cardiac drug Histochrome®, its underlying cardioprotective mechanisms are not well understood. In this study, we investigated the protective role of Ech A against toxic agents that induce death of rat cardiac myoblast H9c2 cells and isolated rat cardiomyocytes. We found that the cardiotoxic agents tert-Butyl hydroperoxide (tBHP, organic reactive oxygen species (ROS) inducer), sodium nitroprusside (SNP; anti-hypertension drug), and doxorubicin (anti-cancer drug) caused mitochondrial dysfunction such as increased ROS level and decreased mitochondrial membrane potential. Co-treatment with Ech A, however, prevented this decrease in membrane potential and increase in ROS level. Co-treatment of Ech A also reduced the effects of these cardiotoxic agents on mitochondrial oxidative phosphorylation and adenosine triphosphate level. These findings indicate the therapeutic potential of Ech A for reducing cardiotoxic agent-induced damage. © 2014 by the authors licensee MDPI.

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APA

Jeong, S. H., Kim, H. K., Song, I. S., Lee, S. J., Ko, K. S., Rhee, B. D., … Han, J. (2014). Echinochrome a protects mitochondrial function in cardiomyocytes against cardiotoxic drugs. Marine Drugs, 12(5), 2922–2936. https://doi.org/10.3390/md12052922

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