Key result
Co-treatment with Echinochrome A prevented mitochondrial dysfunction, including decreased membrane potential and increased ROS levels, induced by cardiotoxic agents in rat cardiomyocytes.
Why the study?
Does Echinochrome A prevent mitochondrial dysfunction induced by cardiotoxic drugs in rat cardiomyocytes?
Does Echinochrome A prevent mitochondrial dysfunction induced by cardiotoxic drugs in rat cardiomyocytes?
Echinochrome A demonstrates therapeutic potential in preventing mitochondrial dysfunction and damage induced by cardiotoxic agents in cardiomyocytes.
Supports Echinochrome A for mitochondrial protection in rat cells; leaves open translation to clinical cardiotoxicity prevention.
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.
No takes yet. Share an insight, caveat, or question.
Jeong et al. (2014) studied Cardiotoxicity. Echinochrome A vs. Cardiotoxic agents alone was evaluated on Mitochondrial dysfunction (ROS level, membrane potential, oxidative phosphorylation, ATP level). Co-treatment with Echinochrome A prevented mitochondrial dysfunction, including decreased membrane potential and increased ROS levels, induced by cardiotoxic agents in rat cardiomyocytes.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: