Key result
Pretreatment with edaravone and benidipine significantly attenuated doxorubicin-induced increases in cardiac biomarkers, TNF-α, Caspase-3 activity, and myocardial infarct size.
Why the study?
Doxorubicin is an effective chemotherapeutic agent whose use is restricted by cardiotoxicity, prompting investigation into whether edaravone, benidipine, or their combination offers cardioprotective effects.
Does pretreatment with edaravone and benidipine protect against doxorubicin-induced cardiotoxicity in a preclinical model?
Does pretreatment with edaravone and benidipine protect against doxorubicin-induced cardiotoxicity in a preclinical model?
Pretreatment with edaravone and benidipine attenuates doxorubicin-induced cardiotoxicity by reducing oxidative stress, apoptosis, and myocardial damage in a preclinical model.
May support experimental cardioprotection by edaravone-benidipine against doxorubicin; leaves open clinical translation.
Background: Doxorubicin (DOX) is a potential chemotherapeutic agent but its use is restricted due to cardiotoxicity. Edaravone is a potent-free radical scavenging agent used in cerebral ischaemia. Benidipine is a triple calcium channel blocker.Objective: We investigated the potential cardioprotective effects of edaravone and benidipine alone and their combination against DOX-induced cardiotoxicity. Cardiotoxicity was induced by administering six equal injections of DOX (2.5 mg/kg) on alternative days for 2 weeks.Result: DOX-treated group showed significant increase level of lipid peroxide and decrease in antioxidant status along with mitochondrial enzymatic activity. Cardiotoxity effect of DOX illustrated by significantly increased the cardiac biomarkers such as Cardiac troponin-I, Brain natriuretic peptide, Creatine kinase-MB in serum. Significant increased activation of TNF-α, Caspase-3 activity and myocardial infarct size in DOX-treated group. Histopathological evaluation also confirmed the DOX-induced cardiotoxicity. Pretreated with edaravone and benidipine was significantly attenuated level of thiobarbituric acid reactive substance, endogenous enzymes, mitochondrial enzyme activities and cardiac biomarkers. Furthermore, pretreated group showed decreased activation of TNF-α, Caspase-3 activity along with reduction in the myocardial infarct size. Histopathological evaluation also strengthened the above results.Conclusion: Taken together these results suggest that the pretreated with edaravone and benidipine have potential protective effect against DOX-induced cardiotoxicity.
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Hassan et al. (2019) studied Doxorubicin-induced cardiotoxicity. Edaravone and benidipine vs. Doxorubicin alone was evaluated on Cardioprotective effects (lipid peroxide, antioxidant status, mitochondrial enzymatic activity, cardiac biomarkers, TNF-α, Caspase-3 activity, myocardial infarct size). Pretreatment with edaravone and benidipine significantly attenuated doxorubicin-induced increases in cardiac biomarkers, TNF-α, Caspase-3 activity, and myocardial infarct size.
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