Diphenyleneiodonium inhibits NF-κB activation and iNOS expression induced by IL-1β: involvement of reactive oxygen species

Aims: In this work, we studied the mechanisms by which diphenyleneiodonium chloride (DPI) inhibits nitric oxide (NO) synthesis induced by the pro-inflammatory cytokine interleukin-1β (IL-1) in bovine articular chondrocytes. To achieve this, we evaluated the ability of DPI to inhibit the expression a...

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Main Authors:	A. Ferreira Mendes, A. Pato Carvalho, M. Margarida Caramona, M. Celeste Lopes
Format:	Article
Language:	English
Published:	Hindawi Limited 2001-01-01
Series:	Mediators of Inflammation
Online Access:	http://dx.doi.org/10.1080/09629350120080401

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spelling	doaj-e4b9fc5a83c84b55b22c87958ba981262020-11-24T21:52:53ZengHindawi LimitedMediators of Inflammation0962-93511466-18612001-01-0110420921510.1080/09629350120080401Diphenyleneiodonium inhibits NF-κB activation and iNOS expression induced by IL-1β: involvement of reactive oxygen speciesA. Ferreira Mendes0A. Pato Carvalho1M. Margarida Caramona2M. Celeste Lopes3Faculty of Pharmacy, Department of Zoology, University of Coimbra, Rua do Norte, Coimbra 3000–295, PortugalCentre for Neurosciences of Coimbra, Department of Zoology, University of Coimbra, Rua do Norte, Coimbra 3000–295, PortugalFaculty of Pharmacy, Department of Zoology, University of Coimbra, Rua do Norte, Coimbra 3000–295, PortugalFaculty of Pharmacy, Department of Zoology, University of Coimbra, Rua do Norte, Coimbra 3000–295, PortugalAims: In this work, we studied the mechanisms by which diphenyleneiodonium chloride (DPI) inhibits nitric oxide (NO) synthesis induced by the pro-inflammatory cytokine interleukin-1β (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 DPI to prevent IL-1-induced NF-κB activation and reactive oxygen species (ROS) production.http://dx.doi.org/10.1080/09629350120080401
collection	DOAJ
language	English
format	Article
sources	DOAJ
author	A. Ferreira Mendes A. Pato Carvalho M. Margarida Caramona M. Celeste Lopes
spellingShingle	A. Ferreira Mendes A. Pato Carvalho M. Margarida Caramona M. Celeste Lopes Diphenyleneiodonium inhibits NF-κB activation and iNOS expression induced by IL-1β: involvement of reactive oxygen species Mediators of Inflammation
author_facet	A. Ferreira Mendes A. Pato Carvalho M. Margarida Caramona M. Celeste Lopes
author_sort	A. Ferreira Mendes
title	Diphenyleneiodonium inhibits NF-κB activation and iNOS expression induced by IL-1β: involvement of reactive oxygen species
title_short	Diphenyleneiodonium inhibits NF-κB activation and iNOS expression induced by IL-1β: involvement of reactive oxygen species
title_full	Diphenyleneiodonium inhibits NF-κB activation and iNOS expression induced by IL-1β: involvement of reactive oxygen species
title_fullStr	Diphenyleneiodonium inhibits NF-κB activation and iNOS expression induced by IL-1β: involvement of reactive oxygen species
title_full_unstemmed	Diphenyleneiodonium inhibits NF-κB activation and iNOS expression induced by IL-1β: involvement of reactive oxygen species
title_sort	diphenyleneiodonium inhibits nf-κb activation and inos expression induced by il-1β: involvement of reactive oxygen species
publisher	Hindawi Limited
series	Mediators of Inflammation
issn	0962-9351 1466-1861
publishDate	2001-01-01
description	Aims: In this work, we studied the mechanisms by which diphenyleneiodonium chloride (DPI) inhibits nitric oxide (NO) synthesis induced by the pro-inflammatory cytokine interleukin-1β (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 DPI to prevent IL-1-induced NF-κB activation and reactive oxygen species (ROS) production.
url	http://dx.doi.org/10.1080/09629350120080401
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Diphenyleneiodonium inhibits NF-κB activation and iNOS expression induced by IL-1β: involvement of reactive oxygen species

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