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Protective Effect of Silymarin against Acrolein-Induced Cardiotoxicity in Mice

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. Studi...

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Autores principales: Taghiabadi, Elahe, Imenshahidi, Mohsen, Abnous, Khalil, Mosafa, Fatemeh, Sankian, Mojtaba, Memar, Bahram, Karimi, Gholamreza
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3535759/
https://www.ncbi.nlm.nih.gov/pubmed/23320028
http://dx.doi.org/10.1155/2012/352091
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author Taghiabadi, Elahe
Imenshahidi, Mohsen
Abnous, Khalil
Mosafa, Fatemeh
Sankian, Mojtaba
Memar, Bahram
Karimi, Gholamreza
author_facet Taghiabadi, Elahe
Imenshahidi, Mohsen
Abnous, Khalil
Mosafa, Fatemeh
Sankian, Mojtaba
Memar, Bahram
Karimi, Gholamreza
author_sort Taghiabadi, Elahe
collection PubMed
description 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.
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spelling pubmed-35357592013-01-14 Protective Effect of Silymarin against Acrolein-Induced Cardiotoxicity in Mice Taghiabadi, Elahe Imenshahidi, Mohsen Abnous, Khalil Mosafa, Fatemeh Sankian, Mojtaba Memar, Bahram Karimi, Gholamreza Evid Based Complement Alternat Med Research Article 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. Hindawi Publishing Corporation 2012 2012-12-18 /pmc/articles/PMC3535759/ /pubmed/23320028 http://dx.doi.org/10.1155/2012/352091 Text en Copyright © 2012 Elahe Taghiabadi et al. https://creativecommons.org/licenses/by/3.0/ 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.
spellingShingle Research Article
Taghiabadi, Elahe
Imenshahidi, Mohsen
Abnous, Khalil
Mosafa, Fatemeh
Sankian, Mojtaba
Memar, Bahram
Karimi, Gholamreza
Protective Effect of Silymarin against Acrolein-Induced Cardiotoxicity in Mice
title Protective Effect of Silymarin against Acrolein-Induced Cardiotoxicity in Mice
title_full Protective Effect of Silymarin against Acrolein-Induced Cardiotoxicity in Mice
title_fullStr Protective Effect of Silymarin against Acrolein-Induced Cardiotoxicity in Mice
title_full_unstemmed Protective Effect of Silymarin against Acrolein-Induced Cardiotoxicity in Mice
title_short Protective Effect of Silymarin against Acrolein-Induced Cardiotoxicity in Mice
title_sort protective effect of silymarin against acrolein-induced cardiotoxicity in mice
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3535759/
https://www.ncbi.nlm.nih.gov/pubmed/23320028
http://dx.doi.org/10.1155/2012/352091
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