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Protective effects of silymarin against bisphenol A-induced hepatotoxicity in mouse liver

Bisphenol A (BPA) is an endocrine-disrupting chemical released into the environment, with severe consequences for human health, including metabolic syndrome and associated pathological conditions. Due to limited information on BPA-induced hepatotoxicity, the present study focused on investigating th...

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Autores principales: Zaulet, Mihaela, Kevorkian, Steliana Elvira Maria, Dinescu, Sorina, Cotoraci, Coralia, Suciu, Maria, Herman, Hildegard, Buburuzan, Laura, Badulescu, Liliana, Ardelean, Aurel, Hermenean, Anca
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5403334/
https://www.ncbi.nlm.nih.gov/pubmed/28450905
http://dx.doi.org/10.3892/etm.2017.4066
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author Zaulet, Mihaela
Kevorkian, Steliana Elvira Maria
Dinescu, Sorina
Cotoraci, Coralia
Suciu, Maria
Herman, Hildegard
Buburuzan, Laura
Badulescu, Liliana
Ardelean, Aurel
Hermenean, Anca
author_facet Zaulet, Mihaela
Kevorkian, Steliana Elvira Maria
Dinescu, Sorina
Cotoraci, Coralia
Suciu, Maria
Herman, Hildegard
Buburuzan, Laura
Badulescu, Liliana
Ardelean, Aurel
Hermenean, Anca
author_sort Zaulet, Mihaela
collection PubMed
description Bisphenol A (BPA) is an endocrine-disrupting chemical released into the environment, with severe consequences for human health, including metabolic syndrome and associated pathological conditions. Due to limited information on BPA-induced hepatotoxicity, the present study focused on investigating the association between BPA-induced toxicity and inflammatory markers in the liver, and how these injuries may be alleviated using the natural agent silymarin, a flavonoid with antioxidant properties obtained from Silybum marianum. Administration of BPA to male CD-1 mice for 10 days caused a significant increase in the number of cells immunopositive for interleukin 6 and tumor necrosis factor-α, pro-inflammatory cytokines that mediate the hepatic inflammatory response. Treatment with 200 mg/kg of silymarin concurrently with BPA for 10 days resulted in a diminished level of pro-inflammatory cytokines and in significantly reduced ultrastructural injuries. Additionally, silymarin was able to restore the significantly decreased glycogen deposits observed following BPA exposure to normal levels, thus favoring hepatic glycogenesis. This study represents the first report of silymarin ability to reduce hepatic lesions and to counteract inflammation caused by BPA in mice. A dose of 200 mg/kg silymarin was sufficient to induce a protective effect against structural and ultrastructural injuries induced by BPA and to lower the levels of pro-inflammatory cytokines observed in murine liver tissue following exposure to BPA.
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spelling pubmed-54033342017-04-27 Protective effects of silymarin against bisphenol A-induced hepatotoxicity in mouse liver Zaulet, Mihaela Kevorkian, Steliana Elvira Maria Dinescu, Sorina Cotoraci, Coralia Suciu, Maria Herman, Hildegard Buburuzan, Laura Badulescu, Liliana Ardelean, Aurel Hermenean, Anca Exp Ther Med Articles Bisphenol A (BPA) is an endocrine-disrupting chemical released into the environment, with severe consequences for human health, including metabolic syndrome and associated pathological conditions. Due to limited information on BPA-induced hepatotoxicity, the present study focused on investigating the association between BPA-induced toxicity and inflammatory markers in the liver, and how these injuries may be alleviated using the natural agent silymarin, a flavonoid with antioxidant properties obtained from Silybum marianum. Administration of BPA to male CD-1 mice for 10 days caused a significant increase in the number of cells immunopositive for interleukin 6 and tumor necrosis factor-α, pro-inflammatory cytokines that mediate the hepatic inflammatory response. Treatment with 200 mg/kg of silymarin concurrently with BPA for 10 days resulted in a diminished level of pro-inflammatory cytokines and in significantly reduced ultrastructural injuries. Additionally, silymarin was able to restore the significantly decreased glycogen deposits observed following BPA exposure to normal levels, thus favoring hepatic glycogenesis. This study represents the first report of silymarin ability to reduce hepatic lesions and to counteract inflammation caused by BPA in mice. A dose of 200 mg/kg silymarin was sufficient to induce a protective effect against structural and ultrastructural injuries induced by BPA and to lower the levels of pro-inflammatory cytokines observed in murine liver tissue following exposure to BPA. D.A. Spandidos 2017-03 2017-01-20 /pmc/articles/PMC5403334/ /pubmed/28450905 http://dx.doi.org/10.3892/etm.2017.4066 Text en Copyright: © Zaulet et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Zaulet, Mihaela
Kevorkian, Steliana Elvira Maria
Dinescu, Sorina
Cotoraci, Coralia
Suciu, Maria
Herman, Hildegard
Buburuzan, Laura
Badulescu, Liliana
Ardelean, Aurel
Hermenean, Anca
Protective effects of silymarin against bisphenol A-induced hepatotoxicity in mouse liver
title Protective effects of silymarin against bisphenol A-induced hepatotoxicity in mouse liver
title_full Protective effects of silymarin against bisphenol A-induced hepatotoxicity in mouse liver
title_fullStr Protective effects of silymarin against bisphenol A-induced hepatotoxicity in mouse liver
title_full_unstemmed Protective effects of silymarin against bisphenol A-induced hepatotoxicity in mouse liver
title_short Protective effects of silymarin against bisphenol A-induced hepatotoxicity in mouse liver
title_sort protective effects of silymarin against bisphenol a-induced hepatotoxicity in mouse liver
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5403334/
https://www.ncbi.nlm.nih.gov/pubmed/28450905
http://dx.doi.org/10.3892/etm.2017.4066
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