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Exp Ther Med. 2017 Mar;13(3):821-828. doi: 10.3892/etm.2017.4066. Epub 2017 Jan 20.

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

Author information

1
Department of Biochemistry and Molecular Biology, University of Bucharest, 050095 Bucharest, Romania.
2
Department of Experimental and Applied Biology, Institute of Life Sciences, 'Vasile Goldiș' Western University of Arad, 310414 Arad, Romania.
3
Department of Hematology, Faculty of Medicine, Pharmacy and Dentistry, 'Vasile Goldiș' Western University of Arad, 310414 Arad, Romania.
4
Department of Cell Biology, Faculty of Medicine, 'Vasile Goldiș' Western University of Arad, 310414 Arad, Romania.
5
Department of Bioengineering of Horti-Viticultural System, University of Agronomical Science and Veterinary Medicine, 011464 Bucharest, Romania.
6
Department of Histology, Faculty of Medicine, 'Vasile Goldiș' Western University of Arad, 310414 Arad, Romania.

Abstract

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.

KEYWORDS:

bisphenol A; hepatoprotection; hepatotoxicity; pro-inflammatory cytokines; silymarin

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