Key result
Catalpol ameliorated doxorubicin-induced cardiotoxicity in mice by inhibiting oxidative stress, myocardial apoptosis, and autophagy via activation of the AKT-mTOR pathway.
Why the study?
Doxorubicin is commonly used as an antitumor drug, but severe cardiotoxicity hinders its clinical application, prompting investigation of the role of catalpol.
Does catalpol ameliorate doxorubicin-induced cardiotoxicity in a mouse model?
Does catalpol ameliorate doxorubicin-induced cardiotoxicity in a mouse model?
Catalpol protects against doxorubicin-induced cardiotoxicity in mice by inhibiting oxidative stress, apoptosis, and autophagy via the AKT-mTOR pathway, suggesting a potential therapeutic strategy.
Hypothesis-generating in mice; does not support clinical use of catalpol for doxorubicin cardiotoxicity.
As a kind of anthracycline, doxorubicin (DOX) is commonly used as an antitumor drug, but its clinical application has been greatly hindered due to its severe cardiotoxicity. Hence, in this study, we investigated the role of catalpol (CTP) and its effect on DOX-induced cardiotoxicity.The cardiac function of mice was evaluated by assessing lactate dehydrogenase, creatine kinase isoenzyme, heart weight to body weight, and heart weight/tibia length levels. Histopathological changes were observed using hematoxylin and eosin staining, and the terminal deoxynucleotidyl transferase dUTP nick end labeling assay was used to examine myocardial apoptosis. Superoxide dismutase (SOD) activity, glutathione (GSH), and malondialdehyde (MDA) levels were measured to confirm the changes in oxidative stress. Western blotting showed the levels of autophagy- and pathway-related proteins. Expression of autophagy marker LC3 was examined using immunofluorescence staining.CTP alleviated DOX-induced cardiac damage in mice. We further observed upregulated SOD and GSH levels, and downregulated MDA level after the CTP treatment in DOX-treated mice, indicating the protective role of CTP against oxidative injury. DOX-induced myocardial apoptosis was also inhibited by CTP treatment in mice. In addition, CTP decreased the levels of Beclin1 and LC3II/LC3I, increased the levels of P62, and activated the protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway in DOX-treated mice.CTP ameliorated DOX-induced cardiotoxicity by inhibiting oxidative stress, myocardial apoptosis, and autophagy via the AKT-mTOR pathway.
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Xie et al. (2023) studied Doxorubicin-induced cardiotoxicity (n=20). Catalpol vs. Normal saline was evaluated. Catalpol ameliorated doxorubicin-induced cardiotoxicity in mice by inhibiting oxidative stress, myocardial apoptosis, and autophagy via activation of the AKT-mTOR pathway.
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