Hesperidin attenuates arsenic trioxide-induced cardiac toxicity in rats

Abstract

Objective: To explore the cardioprotective effect of hesperidin against arsenic trioxide-induced cardiac toxicity in rats. Methods: Cardiac toxicity was induced by oral administration of 4 mg/kg arsenic trioxide for 30 days. Hematological, biochemical, electrocardiography, echocardiography, and histopathological examinations were performed. Results: Hesperidin decreased the neutrophil-to-lymphocyte ratio, calcium, creatine kinase-myoglobin binding, lactate dehydrogenase, IL-6, and lipid peroxidation, as well as increased sodium and potassium concentration and superoxide dismutase and catalase activity in arsenic trioxide-intoxicated rats. Moreover, it reduced peak systolic velocity and end-diastolic velocity while increasing heart rate. Arsenic trioxide-induced histopathological damage to cardiac tissue was prominently alleviated by hesperidin treatment. Conclusions: Hesperidin attenuates arsenic trioxide-induced cardiac toxicity in rats. Therefore, it can be further explored as a cardioprotective agent.

Keywords

• arsenic trioxide; hesperidin; cardiotoxicity; ecg; ck-mb; ldh