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Doxorubicin (DOX) is the most effective and frequently used anticancer drug but its cardiotoxicity is the most important side effect that limits the clinical use of it. This study was designed to investigate the protective role of catechin (CAT) on DOX induced cardiotoxicity. Rats were randomly divided into three groups. Group (I) served as the control. Group (II) served as toxic group, (1.66 mg/kg; i.p.). Group (III) served as protective group, was pretreated with (400 mg CAT/kg; p.o.) for 2 weeks then received DOX with CAT for 12 days. In the present study, administration of DOX induced significant ( p  &lt; 0.001) reductions in cardiac tissue level of reduced glutathione (GSH) and activities of antioxidant enzymes (catalase, superoxide dismutase (SOD), and glutathione-S- transferase (GST)). Moreover, it resulted in a significant ( p  &lt; 0.001) increase in cardiac tissue concentrations of nitric oxide (NO), H 2 O 2  and malondialdehyde (MDA) as well as serum levels of cardiac injury biomarkers (lactate dehydrogenase (LDH), creatine kinase (CK), and creatine kinase-MB (CK-MB)) which were reversed by treatment with CAT. DOX administration induced the loss of myofibrils, hemorrhage, and congested blood vessels. Ultrastructural results revealed loss of myofibrils and intercalated disks and mitochondrial degeneration. All histopathological alterations were reversed by the treatment with CAT. Catechin, as an antioxidant, showed protective effects against DOX cardiotoxicity  via  reducing lipid peroxidation, inflammation, and alleviating apoptosis.

Potential protective effect of catechin on doxorubicin-induced cardiotoxicity in adult male albino rats