Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 김희선 | * |
dc.date.accessioned | 2016-08-28T11:08:56Z | - |
dc.date.available | 2016-08-28T11:08:56Z | - |
dc.date.issued | 2002 | * |
dc.identifier.issn | 0894-1491 | * |
dc.identifier.other | OAK-980 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/218958 | - |
dc.description.abstract | We have previously reported that the production of nitric oxide (NO) in immunostimulated astrocytes was markedly decreased under glucose-deprived conditions. The present study was undertaken to find the contributing factor(s) for the decreased NO production in glucose-deprived immunostimulated astrocytes. NO production in rat primary astrocytes was stimulated for 24-48 h by cotreatment with lipopolysaccharides (1 μg/ml) and interferon-γ (100 U/ml). Decreased NO production in immunostimulated astrocytes by glucose deprivation was mimicked by the glycolytic inhibitor 2-deoxyglucose and reversed by addition of pyruvate and lactate. Glucose deprivation did not alter the expression of inducible nitric oxide synthase (iNOS) in immunostimulated astrocytes. Addition of β-NADPH, but not tetrahydrobiopterine, both of which are essential cofactors for NOS function, completely restored the NO production that was decreased in glucose-deprived immunostimulated astrocytes. Glucose deprivation and immunostimulation synergistically reduced intracellular NADPH level in astrocytes. The results indicate that glucose deprivation decreases NO production in immunostimulated astrocytes by depleting intracellular NADPH, a cofactor of iNOS. © 2002 Wiley-Liss, Inc. | * |
dc.language | English | * |
dc.title | Glucose deprivation decreases nitric oxide production via NADPH depletion in immunostimulated rat primary astrocytes | * |
dc.type | Article | * |
dc.relation.issue | 3 | * |
dc.relation.volume | 37 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 268 | * |
dc.relation.lastpage | 274 | * |
dc.relation.journaltitle | GLIA | * |
dc.identifier.doi | 10.1002/glia.10032 | * |
dc.identifier.wosid | WOS:000174518400008 | * |
dc.identifier.scopusid | 2-s2.0-0036509898 | * |
dc.author.google | Chan Y.S. | * |
dc.author.google | Ji W.C. | * |
dc.author.google | Jae R.R. | * |
dc.author.google | Kwang H.K. | * |
dc.author.google | Choi J.-J. | * |
dc.author.google | Kim H.-S. | * |
dc.author.google | Lee J.-C. | * |
dc.author.google | Lee S.J. | * |
dc.author.google | Hyoung C.K. | * |
dc.author.google | Kim W.-K. | * |
dc.contributor.scopusid | 김희선(57191372551) | * |
dc.date.modifydate | 20240118140922 | * |