Abstract
Objective To evaluate the antioxidant and cardioprotective activities of stem bark extract and solvent fractions of Croton macrostachyus on cyclophosphamide-induced cardiotoxicity in rats. Materials and Methods. DPPH free radical scavenging assay method was used to determine antioxidant activity whereas Sprague-Dawley rats were used to evaluate the cardioprotective activity. Except for the normal control, all groups were subjected to cyclophosphamide (200 mg/kg, i.p.) toxicity on the first day. Enalapril at 10 mg/kg was used as a reference. The hydromethanolic crude extract (100, 200, and 400 mg/kg) and aqueous and ethyl acetate fractions (100 and 200 mg/kg, each) were administered for 10 days. The cardioprotective activities were evaluated using cardiac biomarkers such as Troponin I, aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), total cholesterol (TC), triglyceride (TG), and histopathological studies of heart tissue. Results Crude extract and ethyl acetate and aqueous fractions exhibited free radical scavenging activities at IC50 of 594 μg/mL, 419 μg/mL, and 716 μg/mL, respectively. Crude extract at 400 mg/kg decreased the levels of troponin, AST, ALT, and ALP to 0.29 ± 0.06 ng/mL, 103.00 ± 7.63 U/L, 99.80 ± 6.18 U/L, and 108.80 ± 8.81 U/L, respectively. In addition, ethyl acetate fraction at 200 mg/kg decreased the levels of troponin, AST, ALT, and ALP to 0.22 ± 0.02 ng/mL, 137.00 ± 14.30 U/L, 90.33 ± 6.13 U/L, and 166.67 ± 13.50 U/L, respectively, compared with the cyclophosphamide control group. Conclusions Croton macrostachyus possesses cardioprotective activities and it could be a possible source of treatment for cardiotoxicity induced by cyclophosphamide.
Highlights
Cardiotoxicity induced by drugs poses a serious risk to human health and is becoming an increasingly important concern in cardiooncology [1]
People on cardiotoxic chemotherapy can be considered as a stage A group of heart failure patients [6]
Anticancer drugs are well known to cause a wide array of toxicities, including cardiac damage; these may include cardiac dysfunction leading to heart failure, myocardial ischemia, arrhythmias, hypertension, myocarditis, pericarditis, and thromboembolism [7]
Summary
Cardiotoxicity induced by drugs poses a serious risk to human health and is becoming an increasingly important concern in cardiooncology [1]. Improvements in antineoplastic treatments led to increased overall and progressionfree survival in the management of an increasing number of malignancies [2]. As cancer survival has improved with advancing therapy, late cardiovascular side effects have become an important management issue, in childhood cancers, lymphoma, leukemia, and breast cancer [3]. Cancer survivors, when compared with their healthy counterparts, are at high risk of cardiovascular-related deaths, including myocardial infarction with coronary artery disease, cardiomyopathy with congestive heart failure, and cerebrovascular events [4, 5].
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