Doxorubicin-induced cardiotoxicity in mice; protection by silymarin
Aniss, H., AdLy, C., Said, A., El Sayed, I. (2012). Doxorubicin-induced cardiotoxicity in mice; protection by silymarin. EKB Journal Management System, 48(1), 383-395. doi: 10.21608/ejhm.2012.16242
Heba Abdelnasser Aniss; Camelia AdLy; Ashraf El Metwally Said; Ibrahim Helmy El Sayed. "Doxorubicin-induced cardiotoxicity in mice; protection by silymarin". EKB Journal Management System, 48, 1, 2012, 383-395. doi: 10.21608/ejhm.2012.16242
Aniss, H., AdLy, C., Said, A., El Sayed, I. (2012). 'Doxorubicin-induced cardiotoxicity in mice; protection by silymarin', EKB Journal Management System, 48(1), pp. 383-395. doi: 10.21608/ejhm.2012.16242
Aniss, H., AdLy, C., Said, A., El Sayed, I. Doxorubicin-induced cardiotoxicity in mice; protection by silymarin. EKB Journal Management System, 2012; 48(1): 383-395. doi: 10.21608/ejhm.2012.16242

Doxorubicin-induced cardiotoxicity in mice; protection by silymarin

The Egyptian Journal of Hospital Medicine
Article 5, Volume 48, Issue 1, July 2012, Page 383-395  XML PDF (270.83 K)
Document Type: Original Article
DOI: 10.21608/ejhm.2012.16242
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Authors
Heba Abdelnasser Aniss1; Camelia AdLy1; Ashraf El Metwally Said2; Ibrahim Helmy El Sayed3
1Department of Biochemistry, Faculty of Science (Damietta branch), Mansoura University, Egypt
2Department of Zoology, Faculty of Science (Damietta branch), Mansoura University, Egypt
3Department of Biochemistry, Research Institute for Genetic Engineering and Biotechnology, Menofia University, Egypt.
Abstract
Background: despite its vast utility in clinical oncology, the use of doxorubicin is limited by a potentially fatal cardiomyopathy and congestive heart failure. Free radical formation and antioxidants depletion are mechanisms proposed for this cardiomyopathy. The aim of this study is to compare the potential antioxidative protective effect of silymarin on doxorubicin-induced cardiotoxicity in experimental mice.
Materials and methods: four groups (ten animals in each group) of experimental mice were used as follows: Group 1, mice received only saline (intraperitoneally) and served as a negative control group; Group 2, mice received doxorubicin (intraperitoneally, 5 mg/kg body weight) in three equal injections over a period of two weeks for a cumulative dose of 15 mg/kg body weight; Group 3, mice orally administrated silymarin (200 mg/day/kg body weight) respectively, through an intragastric feeding tube over a period of three weeks; Group 4, mice treated orally with silymarin plus intraperitoneally doxorubicin administration with the same protocol of groups 3 and 4. Serum lactate dehydrogenase (LDH), creatine phosphokinase (CPK), aspartate aminotransferase (ASAT), alanine aminotransferase (ALAT), malondialdehyde (MDA), total nitric oxide (NO), cardiac reduced glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) were measured in all tested groups.
Results: doxorubicin elevated the activities of LDH, CPK, AST, ALT, MDA and NO in the cardiac tissue. Cardiac antioxidant enzymes activities SOD and CAT also increased while GPx activity was decreased. Pre-co-treatment with silymarin prevented the changes induced by doxorubicin administration. These findings demonstrate the cardio-protective effect of silymarin on cardiac antioxidant status during doxorubicin induced cardiac damage in mice.
Conclusion: silymarin could be recommended for further investigation as potentially new indication for clinical application.

Keywords
Doxorubicin; cardiotoxicity; Silymarin; Antioxidant enzymes; Oxidative Stress
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