Effects of β-glucan extracted from Agaricus blazei on the expression of ERCC5, CASP9, and CYP1A1 genes and metabolic profile in HepG2 cells

dc.contributor.authorDa Silva, A. F.
dc.contributor.authorSartori, D.
dc.contributor.authorMacEdo, F. C.
dc.contributor.authorRibeiro, L. R.
dc.contributor.authorFungaro, M. H P
dc.contributor.authorMantovani, M. S.
dc.contributor.institutionUniversidade Estadual de Londrina (UEL)
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-27T11:29:37Z
dc.date.available2014-05-27T11:29:37Z
dc.date.issued2013-06-01
dc.description.abstractThe polysaccharide β-glucan has biological properties that stimulate the immune system and can prevent chronic pathologies, including cancer. It has been shown to prevent damage to DNA caused by the chemical and physical agents to which humans are exposed. However, the mechanism of β-glucan remains poorly understood. The objective of the present study was to verify the protective effect of β-glucan on the expression of the genes ERCC5 (involved in excision repair of DNA damage), CASP9 (involved in apoptosis), and CYP1A1 (involved in the metabolism of xenobiotics) using real-time polymerase chain reaction and perform metabolic profile measurements on the HepG2 cells. Cells were exposed to only benzo[a]pyrene (B[a]P), β-glucan, or a combination of B[a]P with β-glucan. The results demonstrated that 50 μg/mL β-glucan significantly repressed the expression of the ERCC5 gene when compared with the untreated control cells in these conditions. No change was found in the CASP9 transcript level. However, the CYP1A1 gene expression was also induced by HepG2 cells exposed to B[a]P only or in association with β-glucan, showing its effective protector against damage caused by B[a]P, while HepG2 cells exposed to only β-glucan did not show CYP1A1 modulation. The metabolic profiles showed moderate bioenergetic metabolism with an increase in the metabolites involved in bioenergetic metabolism (alanine, glutamate, creatine and phosphocholine) in cells treated with β-glucan and to a lesser extent treated with B[a]P. Thus, these results demonstrate that the chemopreventive activity of β-glucan may modulate bioenergetic metabolism and gene expression. © 2013 The Author(s).en
dc.description.affiliationDepartment of Biology Universidade Estadual de Londrina, Londrina, Paraná
dc.description.affiliationUniversidade Estadual Paulista (UNESP), Rio Claro, São Paulo
dc.description.affiliationUnespUniversidade Estadual Paulista (UNESP), Rio Claro, São Paulo
dc.format.extent647-654
dc.identifierhttp://dx.doi.org/10.1177/0960327112468173
dc.identifier.citationHuman and Experimental Toxicology, v. 32, n. 6, p. 647-654, 2013.
dc.identifier.doi10.1177/0960327112468173
dc.identifier.issn0960-3271
dc.identifier.issn1477-0903
dc.identifier.scopus2-s2.0-84878315329
dc.identifier.urihttp://hdl.handle.net/11449/75559
dc.identifier.wosWOS:000319228700009
dc.language.isoeng
dc.relation.ispartofHuman and Experimental Toxicology
dc.relation.ispartofjcr1.840
dc.relation.ispartofsjr0,559
dc.rights.accessRightsAcesso restrito
dc.sourceScopus
dc.subjectβ-glucan
dc.subjectCASP9
dc.subjectCYP1A1
dc.subjectERCC5
dc.subjectgene expression
dc.subjectalanine
dc.subjectbenzo[a]pyrene
dc.subjectbeta actin
dc.subjectbeta glucan
dc.subjectcaspase 9
dc.subjectcreatine
dc.subjectcytochrome P450 1A1
dc.subjectexcision repair cross complementing protein 5
dc.subjectglutamic acid
dc.subjectphosphorylcholine
dc.subjectunclassified drug
dc.subjectAgaricus blazei
dc.subjectbioenergy
dc.subjectcell strain HepG2
dc.subjectchemoprophylaxis
dc.subjectdrug cytotoxicity
dc.subjectenergy metabolism
dc.subjectgene repression
dc.subjectgenetic transcription
dc.subjecthuman
dc.subjecthuman cell
dc.subjecthuman tissue
dc.subjectnonhuman
dc.subjectpriority journal
dc.subjectreal time polymerase chain reaction
dc.subjectxenobiotic metabolism
dc.titleEffects of β-glucan extracted from Agaricus blazei on the expression of ERCC5, CASP9, and CYP1A1 genes and metabolic profile in HepG2 cellsen
dc.typeArtigo
dcterms.licensehttp://www.sagepub.com/authors/journal/permissions.sp#7
unesp.author.orcid0000-0002-6199-7030[5]
unesp.author.orcid0000-0001-5268-6508[6]

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