Kartogenin Improves Doxorubicin-Induced Cardiotoxicity by Alleviating Oxidative Stress and Protecting Mitochondria

Doxorubicin (DOX) is a common antitumor drug in clinical practice, but its clinical use is limited due to its cardiotoxic side effects. Oxidative stress and mitochondrial damage are involved in DOX-induced cardiotoxicity (DIC). Kartogenin (KGN) has been shown to have a potent ability to resist oxidative stress and maintain mitochondrial homeostasis. But the impact of KGN on DIC has not been reported. This study explores the potential protective effect of KGN on DIC. The effect of KGN on DIC was studied by establishing in vivo and in vitro DIC models. KGN reduced DOX-induced cardiac insufficiency, myocardial injury, oxidative stress damage, and mitochondrial dysfunction. Through network pharmacology and RNA sequencing (RNA-seq), the mechanism of KGN anti-DIC was highly correlated with oxidative stress and mitochondria. These findings suggest that KGN is a valuable and promising strategy for the prevention of doxorubicin cardiotoxicity.