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Titolo:
Diphenyleneiodonium inhibits NF-kappa B activation and iNOS expression induced by IL-1 beta: involvement of reactive oxygen species
Autore:
Mendes, AF; Carvalho, AP; Caramona, MM; Lopes, MC;
Indirizzi:
Univ Coimbra, Fac Pharm, P-3000295 Coimbra, Portugal Univ Coimbra Coimbra Portugal P-3000295 arm, P-3000295 Coimbra, Portugal Univ Coimbra, Ctr Neurosci Coimbra, Dept Zool, P-3000295 Coimbra, PortugalUniv Coimbra Coimbra Portugal P-3000295 ool, P-3000295 Coimbra, Portugal
Titolo Testata:
MEDIATORS OF INFLAMMATION
fascicolo: 4, volume: 10, anno: 2001,
pagine: 209 - 215
SICI:
0962-9351(200108)10:4<209:DINBAA>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE SYNTHASE; NEUTROPHIL NADPH OXIDASE; RAT MESANGIAL CELLS; ARTICULAR CHONDROCYTES; RHEUMATIC DISEASES; ADJUVANT ARTHRITIS; ENDOTHELIAL-CELLS; INTERFERON-GAMMA; GENE-EXPRESSION; SYNOVIAL-FLUID;
Keywords:
reactive oxygen species; flavonoid-containing enzymes; diphenyleneiodonium chloride; pro-inflammatory cytokines; chondrocyte; arthritis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
48
Recensione:
Indirizzi per estratti:
Indirizzo: Lopes, MC Univ Coimbra, Fac Pharm, Rua Norte, P-3000295 Coimbra, Portugal Univ Coimbra Rua Norte Coimbra Portugal P-3000295 bra, Portugal
Citazione:
A.F. Mendes et al., "Diphenyleneiodonium inhibits NF-kappa B activation and iNOS expression induced by IL-1 beta: involvement of reactive oxygen species", MEDIAT INFL, 10(4), 2001, pp. 209-215

Abstract

Aims: In this work, we studied the mechanisms by which diphenylenciodoniumchloride (DPI) inhibits nitric oxide (NO) synthesis induced by the proinflammatory cytokine interteukin-1 beta (IL-1) in bovine articular chondrocytes. To achieve this, we evaluated the ability of DPI to inhibit the expression and activity of the inducible isoform of the NO synthase (iNOS) induced by IL-1. We also studied the ability of DPT to prevent IL-1-induced NF-kappaB activation and reactive oxygen species (ROS) production. Results: Northern and Western blot analysis, respectively, showed that DPIdose-dependently inhibited IL-1-induced iNOS mRNA and protein synthesis inprimary cultures of bovine articular chondrocytes. DPI effectively inhibited NO production (IC50=0.03 +/-0.004 muM), as evaluated by the method of Griess. Nuclear factor-kappa B (NF-kappaB) activation, as evaluated by electrophoretic mobility shift assay, was inhibited by DPI (1-10 muM) in a dose-dependent manner. IL-1-induced ROS production, as evaluated by measurement of dichlorofluorescein fluorescence, was inhibited by DPI at concentrations that also prevented NF-kappaB activation and iNOS expression. Conclusions: DPI inhibits IL-1-induced NO production in chondrocytes; by two distinct mechanisms: (i) by inhibiting NOS activity, and (ii) by preventing iNOS expression through the blockade of NF-kappaB activation. These results also support the involvement of reactive oxygen species in IL-1-induced NF-kappaB activation and expression of NF-kappaB-dependent genes, such asiNOS.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 21/09/20 alle ore 15:58:30