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dc.contributor.authorMa, Zhi-na
dc.contributor.authorLiu, Zhi
dc.contributor.authorWang, Zi
dc.contributor.authorRen, Shen
dc.contributor.authorTang, Shan
dc.contributor.authorWang, Ying-ping
dc.contributor.authorXiao, Sheng-yuan
dc.contributor.authorChen, Chen
dc.contributor.authorLi, Wei
dc.date.accessioned2019-09-10T04:14:21Z
dc.date.available2019-09-10T04:14:21Z
dc.date.issued2017
dc.identifier.issn0278-6915
dc.identifier.doi10.1016/j.fct.2017.10.006
dc.identifier.urihttp://hdl.handle.net/10072/387175
dc.description.abstractNephrotoxicity induced by cisplatin in 30% of all cisplatin treated patients seriously limits its clinical implication as a widely used anticancer agent, and may even cause patients to alter or give up cisplatin therapy. The purpose of this study is to test a protective effect of American ginseng berry extract (AGBE) on cisplatin-induced nephrotoxicity in mice. In this study, the histopathological changes and elevated levels of serum creatinine (CRE) and urea nitrogen (BUN) caused by cisplatin were significantly diminished by AGBE treatment. Oxidative stress caused by cisplatin, evidenced by increases in kidney tissues malondialdehyde (MDA) content, cytochrome P450 E1 (CYP2E1), renal 4-hydroxynonenal (4-HNE) levels and decreases of glutathione (GSH) and superoxide dismutase (SOD) contents, was significantly ameliorated by AGBE pretreatment. The expression levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) were inhibited by AGBE treatment, suggesting a suppression of inflammatory response. Additionally, AGBE clearly inhibited cisplatin-induced activations of nuclear factor-kappa B (NF-κB) and mitogen activated protein kinase (MAPK) signal pathways. Supplementation of cisplatin-intoxicated mice with AGBE also significantly reduced apoptotic protein levels of Bax, cleaved caspase-3, cytochrome c and increased anti-apoptotic protein Bcl-2. These findings highlight nephroprotective effect of AGBE against cisplatin-evoked nephrotoxicity through ROS-mediated MAPK and NF-κB signaling pathways.
dc.description.peerreviewedYes
dc.languageEnglish
dc.language.isoeng
dc.publisherElsevier
dc.relation.ispartofpagefrom62
dc.relation.ispartofpageto73
dc.relation.ispartofjournalFood and Chemical Toxicology
dc.relation.ispartofvolume110
dc.subject.fieldofresearchFood Sciences
dc.subject.fieldofresearchcode0908
dc.subject.keywordsScience & Technology
dc.subject.keywordsLife Sciences & Biomedicine
dc.subject.keywordsFood Science & Technology
dc.subject.keywordsToxicology
dc.subject.keywordsAmerican ginseng berry extract
dc.titleSupplementation of American ginseng berry extract mitigated cisplatin-evoked nephrotoxicity by suppressing ROS-mediated activation of MAPK and NF-kappa B signaling pathways
dc.typeJournal article
dc.type.descriptionC1 - Articles
dcterms.bibliographicCitationMa, Z-N; Liu, Z; Wang, Z; Ren, S; Tang, S; Wang, Y-P; Xiao, S-Y; Chen, C; Li, W, Supplementation of American ginseng berry extract mitigated cisplatin-evoked nephrotoxicity by suppressing ROS-mediated activation of MAPK and NF-kappa B signaling pathways, Food and Chemical Toxicology, 2017, 110, pp. 62-73
dcterms.dateAccepted2017-10-07
dcterms.licensehttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.date.updated2019-09-10T04:09:35Z
dc.description.versionAccepted Manuscript (AM)
gro.rights.copyright© 2017 Elsevier. Licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International Licence (http://creativecommons.org/licenses/by-nc-nd/4.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, providing that the work is properly cited.
gro.hasfulltextFull Text
gro.griffith.authorChen, Chen


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