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pubmed-article:11577997pubmed:abstractTextIn this work, we studied the mechanisms by which diphenyleneiodonium chloride (DPI) inhibits nitric oxide (NO) synthesis induced by the proinflammatory cytokine interleukin-1beta (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-kappaB activation and reactive oxygen species (ROS) production.lld:pubmed
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pubmed-article:11577997pubmed:articleTitleDiphenyleneiodonium inhibits NF-kappaB activation and iNOS expression induced by IL-1beta: involvement of reactive oxygen species.lld:pubmed
pubmed-article:11577997pubmed:affiliationFaculty of Pharmacy, Department of Zoology, University of Coimbra, Portugal.lld:pubmed
pubmed-article:11577997pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:11577997pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed