Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 이지희 | * |
dc.contributor.author | 이경은 | * |
dc.date.accessioned | 2016-08-28T11:08:33Z | - |
dc.date.available | 2016-08-28T11:08:33Z | - |
dc.date.issued | 2000 | * |
dc.identifier.issn | 0300-8177 | * |
dc.identifier.other | OAK-579 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/218724 | - |
dc.description.abstract | Nitric oxide (NO), a reactive nitrogen species, plays an important role in inflammatory lung damage. In the present study, we investigated the role of NO in DNA-binding activity of NF-κB in macrophages stimulated with silica or other inflammatory stimulants. Treatment of mouse macrophages (RAW264.7 cells) with a selective inhibitor of inducible nitric oxide synthase (iNOS), L-N6-(1-iminoethyl) lysine (L-NIL), or a nonselective iNOS inhibitor, Nω-nitro-L-arginine methylester (L-NAME), resulted in inhibition of silica-induced nitric oxide production as well as silica-induced NF-κB activation. L-NIL also effectively inhibited NF-κB activation induced by other inflammatory stimulants, such as lipopolysaccharide (LPS) or muramyl dipeptide (MDP). These inhibitory effects of L-NIL and L-NAME on silica- or LPS-induced NF-κB activation were also observed in primary rat alveolar macrophages. Furthermore, NO generating compounds, such as sodium nitroprusside (SNP) and 3-morpholinosydnonimine (SIN-1), caused a dose-dependent increase in NF-κB activation, which was positively correlated with the level of NO production. Specific inhibitors of protein tyrosine kinase, such as genistein and AG494, prevented NF-κB activation in SNP- or SIN-1 treated cells, suggesting involvement of tyrosine kinase in the NO signaling pathway leading to NF-κB activation. In contrast, inhibitors of protein kinase C or A, such as staurosporine or H89, had no inhibitory effect on SIN-1 induced NF-κB activation. Metalloporphyrins, such as tetrakis (N-methyl-4′-pyridyl) porphyrinato iron (III) (Fe-TMPyP) and Zn-TMPyP which are known to alter NO-dependent activity, markedly inhibited silica- and LPS-induced NF-κB activation. The results suggest that NF-κB activation in macrophages can be induced under certain conditions by nitric oxide and that nitric oxide produced by phagocytes exposed to inflammatory agents may up-regulate the activation of NF-κB. | * |
dc.language | English | * |
dc.title | Nitric oxide up-regulates DNA-binding activity of nuclear factor-κB in macrophages stimulated with silica and inflammatory stimulants | * |
dc.type | Article | * |
dc.relation.issue | 1-2 | * |
dc.relation.volume | 215 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 1 | * |
dc.relation.lastpage | 9 | * |
dc.relation.journaltitle | Molecular and Cellular Biochemistry | * |
dc.identifier.doi | 10.1023/A:1026581301366 | * |
dc.identifier.wosid | WOS:000165642200001 | * |
dc.identifier.scopusid | 2-s2.0-0034507984 | * |
dc.author.google | Kang J.L. | * |
dc.author.google | Lee K. | * |
dc.author.google | Castranova V. | * |
dc.contributor.scopusid | 이지희(7404517577) | * |
dc.contributor.scopusid | 이경은(7409769243) | * |
dc.date.modifydate | 20240116125728 | * |