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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
- Issue Date
- 2007-05-23
- Publisher
- Taylor & Francis
- Citation
- Free Radic Res. 2007 Jun;41(6):720-9.
- Keywords
- Animals ; Antioxidants/pharmacology ; Apoptosis/*drug effects ; Blotting, Western ; Cells, Cultured/drug effects/metabolism ; Comet Assay ; Cricetinae ; Cytoprotection ; Electrophoretic Mobility Shift Assay ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Fibroblasts/cytology/drug effects/metabolism ; Flow Cytometry ; Free Radical Scavengers/pharmacology ; Hydrogen Peroxide/*pharmacology ; Isoflavones/metabolism/*pharmacology ; JNK Mitogen-Activated Protein Kinases/*antagonists & inhibitors/metabolism ; Luciferases/metabolism ; Lung/cytology/drug effects/metabolism ; Mitogen-Activated Protein Kinase 9/metabolism ; Oxidants/*pharmacology ; Oxidative Stress ; Phytoestrogens/pharmacology ; Promoter Regions, Genetic/genetics ; Reactive Oxygen Species/*metabolism ; Transcription 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/10371/24863
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