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Evidence-Based Complementary and Alternative Medicine
Volume 2012 (2012), Article ID 352091, 14 pages
http://dx.doi.org/10.1155/2012/352091
Research Article

Protective Effect of Silymarin against Acrolein-Induced Cardiotoxicity in Mice

1Department of Phamacodynamy and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad 9177948564, Iran
2Pharmaceutical Research Center, Department of Pharmacodynamy and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad 9177948564, Iran
3Department of Pharmaceutical Biotechnology, Mashhad University of Medical Sciences, Mashhad 9177948564, Iran
4Biotechnology Research Center and School of Pharmacy, Mashhad University of Medical Sciences, Mashhad 9177948564, Iran
5Immunology Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad 9177948564, Iran
6Department of Pathology, Imam Reza Hospital, Mashhad University of Medical Sciences, Mashhad 9177948564, Iran
7Medical Toxicology Research Center and School of Pharmacy, Mashhad University of Medical Sciences, Mashhad 9177948564, Iran

Received 16 August 2012; Revised 12 November 2012; Accepted 15 November 2012

Academic Editor: Khalid Rahman

Copyright © 2012 Elahe Taghiabadi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Reactive α,β-unsaturated aldehydes such as acrolein (ACR) are major components of environmental pollutants and have been implicated in the neurodegenerative and cardiac diseases. In this study, the protective effect of silymarin (SN) against cardiotoxicity induced by ACR in mice was evaluated. Studies were performed on seven groups of six animals each, including vehicle-control (normal saline + 0.5% w/v methylcellulose), ACR (7.5 mg/kg/day, gavage) for 3 weeks, SN (25, 50 and 100 mg/kg/day, i.p.) plus ACR, vitamin E (Vit E, 100 IU/kg, i.p.) plus ACR, and SN (100 mg/kg, i.p.) groups. Mice received SN 7 days before ACR and daily thereafter throughout the study. Pretreatment with SN attenuated ACR-induced increased levels of malondialdehyde (MDA), serum cardiac troponin I (cTnI), and creatine kinase-MB (CK-MB), as well as histopathological changes in cardiac tissues. Moreover, SN improved glutathione (GSH) content, superoxide dismutase (SOD), and catalase (CAT) activities in heart of ACR-treated mice. Western blot analysis showed that SN pretreatment inhibited apoptosis provoked by ACR through decreasing Bax/Bcl-2 ratio, cytosolic cytochrome c content, and cleaved caspase-3 level in heart. In conclusion, SN may have protective effects against cardiotoxicity of ACR by reducing lipid peroxidation, renewing the activities of antioxidant enzymes, and preventing apoptosis.