Key result
Eleutheroside E reduces doxorubicin-induced cardiotoxicity in vivo by inhibiting ferroptosis to improve cardiac function.
Why the study?
Eleutheroside E has established cardioprotective properties, but its potential against doxorubicin-induced cardiotoxicity had not been investigated.
Does Eleutheroside E mitigate doxorubicin-induced cardiotoxicity in preclinical models?
Does Eleutheroside E mitigate doxorubicin-induced cardiotoxicity in preclinical models?
Eleutheroside E demonstrates therapeutic potential in mitigating doxorubicin-induced cardiotoxicity by suppressing ferroptosis through the Nrf2 pathway.
Should not yet change clinical practice; extends evidence for Nrf2/SLC7A11/GPX4 activation to inhibit ferroptosis in doxorubicin cardiotoxicity.
Doxorubicin (DOX)-induced cardiotoxicity significantly impairs cancer patient survival rates. Eleutheroside E (EE), a polyphenolic compound with established cardioprotective properties against high-altitude myocardial injury and ischemia/reperfusion damage, has not previously been investigated in the context of DOX-induced cardiac toxicity. This study aimed to elucidate the therapeutic potential of EE against DOX-associated cardiotoxicity and its underlying mechanisms. Cardiomyocyte viability was quantified using the CCK-8 assay and Hoechst 33342/PI dual staining. Cardiac function was evaluated by echocardiography. Morphological alterations in cardiomyocytes were analyzed through phalloidin, hematoxylin-eosin (H&E), and wheat germ agglutinin staining. Ferroptosis-related biomarkers including malondialdehyde (MDA), Ptgs2 mRNA levels, Fe²⁺ concentration, and lipid peroxidation were assessed respectively. EE administration attenuated DOX-induced cardiomyocyte atrophy in-vitro and improved cardiac function in-vivo. Mechanistically, EE counteracted DOX-mediated suppression of Nrf2 expression and inhibited ferroptosis via activation of the Nrf2/SLC7A11/GPX4 signaling axis. siRNA-mediated Nrf2 knockdown partly abolished EE's cardioprotective effects. These findings conclusively demonstrate that EE mitigates DOX-induced cardiotoxicity through Nrf2-dependent ferroptosis regulation, highlighting its therapeutic potential for preventing chemotherapy-associated cardiac complications.
No takes yet. Share an insight, caveat, or question.
Sun et al. (2026) studied this question. Eleutheroside E reduced doxorubicin-induced cardiotoxicity by activating Nrf2/SLC7A11/GPX4 signaling and inhibiting ferroptosis, improving cardiac function in vivo.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: