Allicin and L-carnitine as Preventive Agents Against Doxorubicin-induced Cardiac Damage in Rats : ALC and LC protect against DOX induced cardiac toxicity
نویسندگان
1 Department of Pharmacology, Faculty of Veterinary Medicine, Cairo University, Giza, Egypt.
2 Department of Biotechnology, College of Science, Taif University, Taif, Saudi Arabia.
3 Department of Family Medicine, Prince Mansour Military Hospital, Taif, Saudi Arabia.
4 Department of Pharmacology and Toxicology, Faculty of Pharmaceutical Sciences and Drug Manufacturing, Misr University for Science and Technology, Giza, Egypt.
5 Department of Pharmacology, Faculty of Veterinary Medicine, Benha University, Qaliobiya, Egypt.
6 Department of Forensic Medicine and Toxicology, Faculty of Veterinary Medicine, Matrouh University, Matrouh, Egypt.
7 Department of Pharmacology and Toxicology, College of Pharmacy, Taif University, Taif, Saudi Arabia.
doi
10.32598/ijmtfm.v14i03.45510چکیده
Background: Doxorubicin (DOX) is a potent anthracycline chemotherapy agent widely employed to treat various malignancies, such as cancers and this study sought to determine how allicin (ALC) and or L-carnitine (LC) affect DOX-induced cardiotoxicity in rats.Methods: In this study, the possible alleviative role of ALC (20 mg/kg/day orally (PO)) or LC (100 mg/kg/day PO) or the combined treatment of both ALC and LC (with the previously mentioned dosages) was evaluated against the cardiotoxic effect of a widely used chemotherapeutic agent, DOX (20 mg DOX /kg intraperitoneal injection (IP) as a single dose) in rats in 30 days experiment. Results: The results revealed that ALC and LC significantly suppressed the DOX-induced increment in serum levels of cardiac damage biomarkers, such as lactate dehydrogenase (LDH), creatine kinase (CK) and creatine kinase-megabyte (CK-MB). Moreover, DOX-associated oxidative stress, including the elevation in malondialdehyde (MDA) level and reduced activity of antioxidant enzymes, such as catalase (CAT) and superoxide dismutase (SOD) and the level of reduced glutathione (GSH) was corrected in ALC and or LC treated groups. Furthermore, DOX-induced cardiomyopathy showed significant pathological changes, including myocyte degeneration, vacuolization, interstitial edema, and focal necrosis. Nevertheless, the histopathological lesions were corrected in the treated groups mostly in the combined treatment with ALC plus LC. Compared to ALC and LC, ALC plus LC was more effective at restoring the cardiac injury biomarkers, inhibiting cardiac oxidative damage and preserving the cardiac architecture. Conclusions: Conclusively, the study results evidenced the beneficial role of the combined treatment with ALC plus LC in mitigating DOX-induced cardiotoxicity.
