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Roles of Reactive Oxygen Species, NF-κB, and Peroxiredoxins in Glycochenodeoxycholic Acid-Induced Rat Hepatocytes Death
DC Field | Value | Language |
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dc.contributor.author | 추상희 | - |
dc.date.accessioned | 2015-07-15T16:35:47Z | - |
dc.date.available | 2015-07-15T16:35:47Z | - |
dc.date.issued | 2003 | - |
dc.identifier.issn | 0031-7012 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/113214 | - |
dc.description.abstract | The aim of this study was to determine the roles of reactive oxygen species (ROS), NF-κB and antioxidants in glycochenodeoxycholic acid (GCDC, 0–400 μmol/l, 0.5– 3 h)-induced hepatocytes death. The differential uptake of ethidium bromide and acridine orange revealed that apoptotic death occurred dose-dependently in GCDC-treated hepatocytes whereas necrotic death was prominent especially at higher GCDC concentrations (≥200 μmol/l). ROS generation measured fluorometrically either by a confocal laser microscope or by a microplate fluorescence reader was increased dose-dependently. The dose-dependent NF-κB activation with the significant IκB-α decrease preceded both hepatocyte cell death and the alteration of antioxidant enzymes. The Cu/Zn-SOD level among several antioxidants, we checked, remained unchanged. In contrast, the catalase level and its enzymatic activity were markedly decreased only at 400 μmol/l. The Prx I and Prx II, newly defined antioxidant enzymes reducing H2O2 levels were decreased at the 200 and 400 μmol/l. These observations point to ROS generation in the GCDC-treated hepatocyte as the proximate event that triggers NF-κB activation, IκB-α proteolysis, Prx depletion, and finally cell death. And oxidative stress may be more related to necrotic cell death in GCDC-treated hepatocytes. | - |
dc.description.statementOfResponsibility | open | - |
dc.relation.isPartOf | PHARMACOLOGY | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Animals | - |
dc.subject.MESH | Apoptosis/drug effects* | - |
dc.subject.MESH | Bile Acids and Salts/adverse effects* | - |
dc.subject.MESH | Catalase/metabolism | - |
dc.subject.MESH | Cells, Cultured | - |
dc.subject.MESH | GlycochenodeoxycholicAcid/toxicity* | - |
dc.subject.MESH | Hepatocytes/drug effects* | - |
dc.subject.MESH | Hepatocytes/metabolism* | - |
dc.subject.MESH | Homeodomain Proteins/metabolism | - |
dc.subject.MESH | Male | - |
dc.subject.MESH | NF-kappa B/physiology* | - |
dc.subject.MESH | Peroxidases/physiology* | - |
dc.subject.MESH | Peroxiredoxins | - |
dc.subject.MESH | Rats | - |
dc.subject.MESH | Rats, Sprague-Dawley | - |
dc.subject.MESH | ReactiveOxygenSpecies/metabolism* | - |
dc.title | Roles of Reactive Oxygen Species, NF-κB, and Peroxiredoxins in Glycochenodeoxycholic Acid-Induced Rat Hepatocytes Death | - |
dc.type | Article | - |
dc.contributor.college | College of Nursing (간호대학) | - |
dc.contributor.department | Dept. of Nursing Environment Systems (임상간호과학과) | - |
dc.contributor.googleauthor | Chu S.H. | - |
dc.contributor.googleauthor | Lee-Kang J. | - |
dc.contributor.googleauthor | Lee K. | - |
dc.contributor.googleauthor | Lee K.-H. | - |
dc.identifier.doi | 10.1159/000071244 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A04232 | - |
dc.relation.journalcode | J02509 | - |
dc.identifier.eissn | 1423-0313 | - |
dc.identifier.pmid | 12886025 | - |
dc.identifier.url | http://www.karger.com/Article/FullText/71244 | - |
dc.contributor.alternativeName | Choo, Sang Hee | - |
dc.contributor.affiliatedAuthor | Choo, Sang Hee | - |
dc.rights.accessRights | not free | - |
dc.citation.volume | 69 | - |
dc.citation.number | 1 | - |
dc.citation.startPage | 12 | - |
dc.citation.endPage | 19 | - |
dc.identifier.bibliographicCitation | PHARMACOLOGY, Vol.69(1) : 12-19, 2003 | - |
dc.identifier.rimsid | 54213 | - |
dc.type.rims | ART | - |
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