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.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
