Key result
Cardamonin protected against doxorubicin-induced cardiotoxicity in mice by activating Nrf2 signaling, suppressing oxidative stress and inflammation, and improving cardiac function.
Why the study?
The molecular mechanisms underlying doxorubicin-induced cardiomyopathy are not completely clarified, and disease-specific therapeutic strategies are lacking.
Does cardamonin protect against doxorubicin-induced cardiotoxicity in a mouse model?
Population
DOX-treated mouse cardiomyocytes and a DOX-induced cardiotoxicity mouse model
Comparison
Cardamonin treatment vs DOX alone
Design
Preclinical in vitro and animal study
Authors
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May support Nrf2-targeted adjuncts with doxorubicin; leaves open translation beyond this mouse model.
Does cardamonin protect against doxorubicin-induced cardiotoxicity in a mouse model?
Cardamonin demonstrates potential as a therapeutic strategy to prevent doxorubicin-induced cardiomyopathy by activating the Nrf2-related cytoprotective system in a preclinical model.
Wang et al. (2019) studied Doxorubicin-induced cardiotoxicity. Cardamonin vs. Doxorubicin alone was evaluated on Oxidative stress, apoptosis, inflammatory response, and cardiac function. Cardamonin protected against doxorubicin-induced cardiotoxicity in mice by activating Nrf2 signaling, suppressing oxidative stress and inflammation, and improving cardiac function.
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