Journal
MARINE DRUGS
Volume 12, Issue 5, Pages 2922-2936Publisher
MDPI
DOI: 10.3390/md12052922
Keywords
echinochrome A; mitochondrial function; cardiotoxic drugs; SNP; tBHP; doxorubicin
Categories
Funding
- Priority Research Centers Program through the National Research Foundation of Korea (NRF) - Ministry of Education, Science and Technology, Republic Korea [2010-0020224, 2012R1A2A1A03007595, 2011-0028925]
Ask authors/readers for more resources
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 (R), 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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available