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BioMed Research International
Volume 2018, Article ID 6056948, 8 pages
https://doi.org/10.1155/2018/6056948
Research Article

Protective Effects of Silymarin and Silibinin against DNA Damage in Human Blood Cells

1Laboratório de Radiobiologia e Mutagênese, Instituto de Ciências Biológicas, Universidade Federal de Goiás, Campus II, Goiânia, GO, Brazil
2Laboratório de Mutagênese (LABMUT), Instituto de Ciências Biológicas, Universidade Federal de Goiás, Campus II, Goiânia, GO, Brazil
3Laboratório de Biotecnologia, Câmpus Henrique Santillo, Universidade Estadual de Goiás, Anápolis, GO, Brazil
4Núcleo de Pesquisas Replicon, Escola de Ciências Agrárias e Biológicas, Pontifícia Universidade Católica de Goiás, Goiânia, GO, Brazil

Correspondence should be addressed to Lee Chen-Chen; rb.moc.oohay@ogeelnehc

Received 11 May 2018; Revised 25 July 2018; Accepted 2 September 2018; Published 2 October 2018

Guest Editor: Claudio Tabolacci

Copyright © 2018 Flávio Fernandes Veloso Borges 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

Silymarin (SM), a standardized extract derived from Silybum marianum (L.) Gaertn, is primarily composed of flavonolignans, with silibinin (SB) as its major active constituent. The present study aimed to evaluate the antigenotoxic activities of SM and SB using the alkaline comet assay in whole blood cells and to assess their effects on the expression of genes associated with carcinogenesis and chemopreventive processes. Different concentrations of SM or SB (1.0, 2.5, 5.0, and 7.5 mg/ml) were used in combination with the DNA damage-inducing agent methyl methanesulfonate (MMS, 800 μM) to evaluate their genoprotective potential. To investigate the role of SM and SB in modulating gene expression, we performed quantitative real-time PCR (qRT-PCR) analysis of five genes that are known to be involved in DNA damage, carcinogenesis, and/or chemopreventive mechanisms. Treatment with SM or SB was found to significantly reduce the genotoxicity of MMS, upregulate the expression of PTEN and BCL2, and downregulate the expression of BAX and ABL1. We observed no significant changes in ETV6 expression levels following treatment with SM or SB. In conclusion, both SM and SB exerted antigenotoxic activities and modulated the expression of genes related to cell protection against DNA damage.