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Inhibitory effects of glycitein on hydrogen peroxide induced cell damage by scavenging reactive oxygen species and inhibiting c-Jun N-terminal kinase

Cited 26 time in Web of Science Cited 25 time in Scopus
Authors

Kang, Kyoung Ah; Zhang, Rui; Piao, Mei Jing; Lee, Kyoung Hwa; Kim, Bum Joon; Kim, So Young; Kim, Hee Sun; Kim, Dong Hyun; You, Ho Jin; Hyun, Jin Won

Issue Date
2007-05-23
Publisher
Taylor & Francis
Citation
Free Radic Res. 2007 Jun;41(6):720-9.
Keywords
AnimalsAntioxidants/pharmacologyApoptosis/*drug effectsBlotting, WesternCells, Cultured/drug effects/metabolismComet AssayCricetinaeCytoprotectionElectrophoretic Mobility Shift AssayExtracellular Signal-Regulated MAP Kinases/metabolismFibroblasts/cytology/drug effects/metabolismFlow CytometryFree Radical Scavengers/pharmacologyHydrogen Peroxide/*pharmacologyIsoflavones/metabolism/*pharmacologyJNK Mitogen-Activated Protein Kinases/*antagonists & inhibitors/metabolismLuciferases/metabolismLung/cytology/drug effects/metabolismMitogen-Activated Protein Kinase 9/metabolismOxidants/*pharmacologyOxidative StressPhytoestrogens/pharmacologyPromoter Regions, Genetic/geneticsReactive Oxygen Species/*metabolismTranscription Factor AP-1/genetics/metabolism
Abstract
The present study investigated the cytoprotective properties of glycitein, a metabolite formed by the transformation of glycitin by intestinal microflora, against oxidative stress. Glycitein was found to scavenge intracellular reactive oxygen species (ROS), and 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical, and thereby preventing lipid peroxidation and DNA damage. Glycitein inhibited apoptosis of Chinese hamster lung fibroblast (V79-4) cells exposed to hydrogen peroxide (H(2)O(2)) via radical scavenging activity. Glycitein abrogated the activation of c-Jun N-terminal kinase (JNK) induced by H(2)O(2) treatment and inhibited DNA binding activity of activator protein-1 (AP-1), a downstream transcription factor of JNK. Taken together, these findings suggest that glycitein protected H(2)O(2) induced cell death in V79-4 cells by inhibiting ROS generation and JNK activation.
ISSN
1071-5762 (Print)
Language
English
URI
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17516245

https://hdl.handle.net/10371/28482
DOI
https://doi.org/10.1080/10715760701241618
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