3.8 Article

Betanin and Allicin Ameliorate Adriamycin-Induced Cardiotoxicity in Rats by Ameliorating Cardiac Ischemia and Improving Antioxidant Efficiency

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SCIENCEDOMAIN INT
DOI: 10.9734/JPRI/2021/v33i731200

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Adriamycin; allicin; betanin; cardiotoxicity; electrocardiography

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This study investigated the protective effects of betanin and allicin against ADR-induced cardiotoxicity. The results showed that pre-administration of betanin and allicin can alleviate ADR-induced heart damage, suggesting their potential as promising cardioprotective agents.
Aims: To investigate the protective effects of betanin and allicin against adriamycin (ADR)-induced cardiotoxicity. Study Design: Experimental animal model. Place and Duration of Study: King Abdul-Aziz University, Jeddah, Saudi Arabia; 10 days. Methodology: Adult female Wistar rats were allocated to the following groups (n = 10 per group): Control, received water, a standard diet for 10 days and i.p normal saline on day 8; ADR, intraperitoneal injection with 15 mg/kg ADR as a single dose on day 8; ADR+BE, betanin (20 mg/kg) administration followed by i.p. injection of ADR (15 mg/kg); ADR+ALL, allicin (20 mg/kg) administration followed by i.p. injection of ADR; and ADR+BE+ALL, equal volumes of betanin and allicin followed by ADR (15 mg/kg). Hemodynamic characteristics of the cardiovascular system and electrocardiography were evaluated. Blood samples were obtained to assess cardiac enzymes; cardiac homogenates were processed to analyze oxidative and antioxidant parameters and low-grade inflammatory indicators. Histopathological evaluation of heart tissues was also conducted. Results: Rats pre-administered betanin and allicin were protected from ADR-associated ischemia based on the significant (P < .05) shortening of QT, QT(C) interval, QRS, and T peak Tend interval compared with the ADR group. Betanin and allicin pre-treatment significantly decreased the ADR-induced elevated serum creatine kinase-MB and lactate dehydrogenase levels. ADR-elevated cardiac oxidative parameters, along with the serum concentrations of the tumor necrosis factor-alpha and the cardiac transforming growth factor-beta, were significantly inhibited by betanin and allicin. Histopathological findings confirmed the biochemical results. Betanin and allicin reduced ADR-induced heart damage by inhibiting several pathways, including those of oxidative stress and inflammation. Conclusion: Betanin and allicin may be promising cardioprotective agents owing to their antioxidant and cytoprotective properties and could thus be used as adjuvant treatment for cancer therapy.

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