Related Experiment Video
Updated: Aug 28, 2025

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish
Published on: June 7, 2018
Didymin attenuates doxorubicin-induced cardiotoxicity by inhibiting oxidative stress
Rongchang Chen1, Guibo Sun1, Lijiao Xu1
1Institute of Medicinal Plant Development, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100193, China.
Objective:
This study was designed to investigate the protective effects of didymin (Did) on doxorubicin (DOX)-induced cardiotoxicity.
Methods:
After pretreatment with Did (2, 4, 8 mg/kg intraperitoneal i.p.) for 7 d, the male C57 mice were injected with single dose of DOX (20 mg/kg i.p.). The cardioprotective effect of Did was observed on the 7th day after DOX treatment.
Results:
DOX delayed body growth and caused cardiac tissue injury, oxidative stress, and mitochondrial dysfunction. Similar experiments in H9C2 cardiomyocytes showed that DOX reduced cell viability, increased generation of reactive oxygen species (ROS) and fragmentation of DNA, decreased mitochondrial membrane potential, and induced cardiomyocyte apoptosis. However, all of these adverse effects were suppressed by Did pretreatment. Did increased protein expression of glutamate-L-cysteine ligase catalytic subunit (GCL), heme oxygenase 1 (HO-1), and nuclear factor erythroid 2-related factor 2 (Nrf2). Besides, Did also induced activation of PI3K/AKT.
Conclusion:
These findings indicated Did prevented DOX-induced cardiac injury and apoptosis via activating PI3K/AKT/Nrf2 signaling pathway.
More Related Videos
Related Concept Videos
Heart Failure Drugs: Inotropic Agents
Cardiomyopathy II: Dilated Cardiomyopathy
Electron Transport Chain: Complex I and II
ROS generation is regulated and maintained at moderate levels necessary...
Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers
Cardiomyopathy IV: Restrictive Cardiomyopathy
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

