Effects of tenidap on intracellular signal transduction and the induction of proinflammatory cytokines: a review
Identifieur interne : 002A02 ( Main/Exploration ); précédent : 002A01; suivant : 002A03Effects of tenidap on intracellular signal transduction and the induction of proinflammatory cytokines: a review
Auteurs : Jan BondesonSource :
- General Pharmacology [ 0306-3623 ] ; 1996.
English descriptors
- Teeft :
- Acidification, Arachidonate, Arachidonate release, Arthrit, Assay, Blackburn, Bondeson, Breedveld, Chondrocytes, Clinical studies, Collagenase, Cyclooxygenase, Cyclooxygenase inhibition, Cytokine, Dmards, Elisa, Fetal, Fetal calf serum, Fibroblast, Higher concentrations, Inositol, Intracellular, Kinase, Leukotriene, Littman, Macrophage, Mcniff, Monocyte, Mrna, Naproxen, Neutrophil, Nsaid, Otterness, Pelletier, Pharmac, Phospholipase, Phosphorylation, Piroxicam, Polymorphonuclear, Prostaglandin, Protein synthesis, Receptor, Rheum, Rheumatoid, Rheumatoid arthritis, Rheumatol, Sipe, Sundler, Suppl, Synovial, Tenidap, Transduction, Zymosan.
Abstract
Abstract: Tenidap is a novel, once-daily antirheumatic drug which has shown promising results against rheumatoid arthritis in extensive clinical trials. It combines NSAID-like cyclooxygenase inhibition with suppression of the acute phase response. In macrophages, tenidap inhibits the lipopolysaccharide-induced synthesis of interleukins-I and -6, but it tends to potentiate the lipopolysaccharide-induced synthesis of tumor necrosis factor α, due to its cyclooxygenase inhibition. In macrophages, tenidap is a potent inhibitor of zymosan-induced responses, not only the induction of proinflammatory cytokines, but also arachidonate mobilization, protein phosphorylation, and inositol phosphate formation, possibly through interference with the receptor-mediated upregulation of phospholipase C. Tenidap also acts as an intracellular acidifier in many cell types, which may explain at least some of its other effects. Recent studies have indicated that, in addition to modulation of prostanoid and cytokine formation, tenidap has many other effects beneficial in rheumatic disease. It has been shown to inhibit bone resorption, neutrophil adhesion and degranulation, the interleukin-l-induced suppression of glycosaminoglycan synthesis, as well as the production of active metalloproteinases from chondrocytes.
Url:
DOI: 10.1016/0306-3623(95)02049-7
Affiliations:
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It combines NSAID-like cyclooxygenase inhibition with suppression of the acute phase response. In macrophages, tenidap inhibits the lipopolysaccharide-induced synthesis of interleukins-I and -6, but it tends to potentiate the lipopolysaccharide-induced synthesis of tumor necrosis factor α, due to its cyclooxygenase inhibition. In macrophages, tenidap is a potent inhibitor of zymosan-induced responses, not only the induction of proinflammatory cytokines, but also arachidonate mobilization, protein phosphorylation, and inositol phosphate formation, possibly through interference with the receptor-mediated upregulation of phospholipase C. Tenidap also acts as an intracellular acidifier in many cell types, which may explain at least some of its other effects. Recent studies have indicated that, in addition to modulation of prostanoid and cytokine formation, tenidap has many other effects beneficial in rheumatic disease. It has been shown to inhibit bone resorption, neutrophil adhesion and degranulation, the interleukin-l-induced suppression of glycosaminoglycan synthesis, as well as the production of active metalloproteinases from chondrocytes.</div></front></TEI><affiliations><list></list><tree><noCountry><name sortKey="Bondeson, Jan" sort="Bondeson, Jan" uniqKey="Bondeson J" first="Jan" last="Bondeson">Jan Bondeson</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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