Antimalarial Drugs Inhibit Phospholipase A2 Activation and Induction of Interleukin lβ and Tumor Necrosis Factor α in Macrophages: Implications for Their Mode of Action in Rheumatoid Arthritis
Identifieur interne : 002838 ( Main/Exploration ); précédent : 002837; suivant : 002839Antimalarial Drugs Inhibit Phospholipase A2 Activation and Induction of Interleukin lβ and Tumor Necrosis Factor α in Macrophages: Implications for Their Mode of Action in Rheumatoid Arthritis
Auteurs : Jan Bondeson [Suède] ; Roger Sundler [Suède]Source :
- General Pharmacology [ 0306-3623 ] ; 1998.
English descriptors
- KwdEn :
- Teeft :
- Actin, Actin mrna, Antimalarial, Antimalarial drugs, Arachidonate, Arachidonate mobilization, Arachidonate release, Arachidonic, Arachidonic acid, Arachidonic acid release, Arthritis rheum, Assay, Bondeson, Bovine serum albumin, Chloroquine, Culture medium, Cytokine, Cytokine mrna expression, Differential effects, Eicosanoid, Glycerophosphoinositol, Hydroxychloroquine, Incubation time, Inhibitory effect, Inositol, Inositol phosphates, Intracellular, Kinase, Lipid, Lipid phases, Macrophage, Macrophage phospholipase, Macrophage signal transduction, Mouse macrophages, Mrna, Open circles, Overnight preincubation, Pge2, Pharmac, Phospholipase, Preincubation, Proinflammatory, Proinflammatory cytokines, Prostanoid formation, Protein kinase, Protein levels, Quinacrine, Rheumatic disease, Rheumatoid, Rheumatoid arthritis, Separate experiments, Significant inhibition, Slight increase, Smaller amounts, Solid circles, Sundler, Superoxide release, Total inositol radioactivity, Total mrna, Transduction, Tumor necrosis factor, Western analysis, Zymosan.
Abstract
Abstract: 1. The effects of antimalarial drugs on the intracellular signaling leading to activation of the phospholipase C and phospholipase A2 pathways and the induction of proinflammatory cytokines have been studied in mouse macrophages. 2. Both chloroquine and quinacrine, and to a lesser extent hydroxychloroquine, inhibited arachidonate release and eicosanoid formation induced by phorbol diester. This inhibition was due to that of the activation of the arachidonate-mobilizing phospholipase A2. 3. All three antimalarials potently inhibited arachidonate release induced by zymosan. They also inhibited the zymosan-induced formation of inositol phosphates, which hints that an inhibitory effect at the phospholipase C level might explain the inhibition of the response to zymosan. 4. Quinacrine, and to a lesser extent chloroquine, has an inhibitory effect on the lipopolysaccharide- or zymosan-induced expression of interleukin 1β and tumor necrosis factor α, both at the mRNA and protein levels. This, in particular, has important implications for the mode of action of these compounds in rheumatoid arthritis.
Url:
DOI: 10.1016/S0306-3623(97)00269-3
Affiliations:
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Box 94, S-221 00 Lund</wicri:regionArea><wicri:noRegion>S-221 00 Lund</wicri:noRegion></affiliation></author><author><name sortKey="Sundler, Roger" sort="Sundler, Roger" uniqKey="Sundler R" first="Roger" last="Sundler">Roger Sundler</name><affiliation wicri:level="1"><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Cell and Molecular Biology, Lund University, P.O. Box 94, S-221 00 Lund</wicri:regionArea><wicri:noRegion>S-221 00 Lund</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">General Pharmacology</title><title level="j" type="abbrev">GPH</title><idno type="ISSN">0306-3623</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1998">1998</date><biblScope unit="volume">30</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="357">357</biblScope><biblScope unit="page" to="366">366</biblScope></imprint><idno type="ISSN">0306-3623</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0306-3623</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antimalarials</term><term>arachidonate</term><term>chloroquine</term><term>hydroxychloroquine</term><term>interleukin 1</term><term>phospholipase A2</term><term>quinacrine</term><term>tumor necrosis factor α</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Actin</term><term>Actin mrna</term><term>Antimalarial</term><term>Antimalarial drugs</term><term>Arachidonate</term><term>Arachidonate mobilization</term><term>Arachidonate release</term><term>Arachidonic</term><term>Arachidonic acid</term><term>Arachidonic acid release</term><term>Arthritis rheum</term><term>Assay</term><term>Bondeson</term><term>Bovine serum albumin</term><term>Chloroquine</term><term>Culture medium</term><term>Cytokine</term><term>Cytokine mrna expression</term><term>Differential effects</term><term>Eicosanoid</term><term>Glycerophosphoinositol</term><term>Hydroxychloroquine</term><term>Incubation time</term><term>Inhibitory effect</term><term>Inositol</term><term>Inositol phosphates</term><term>Intracellular</term><term>Kinase</term><term>Lipid</term><term>Lipid phases</term><term>Macrophage</term><term>Macrophage phospholipase</term><term>Macrophage signal transduction</term><term>Mouse macrophages</term><term>Mrna</term><term>Open circles</term><term>Overnight preincubation</term><term>Pge2</term><term>Pharmac</term><term>Phospholipase</term><term>Preincubation</term><term>Proinflammatory</term><term>Proinflammatory cytokines</term><term>Prostanoid formation</term><term>Protein kinase</term><term>Protein levels</term><term>Quinacrine</term><term>Rheumatic disease</term><term>Rheumatoid</term><term>Rheumatoid arthritis</term><term>Separate experiments</term><term>Significant inhibition</term><term>Slight increase</term><term>Smaller amounts</term><term>Solid circles</term><term>Sundler</term><term>Superoxide release</term><term>Total inositol radioactivity</term><term>Total mrna</term><term>Transduction</term><term>Tumor necrosis factor</term><term>Western analysis</term><term>Zymosan</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: 1. The effects of antimalarial drugs on the intracellular signaling leading to activation of the phospholipase C and phospholipase A2 pathways and the induction of proinflammatory cytokines have been studied in mouse macrophages. 2. Both chloroquine and quinacrine, and to a lesser extent hydroxychloroquine, inhibited arachidonate release and eicosanoid formation induced by phorbol diester. This inhibition was due to that of the activation of the arachidonate-mobilizing phospholipase A2. 3. All three antimalarials potently inhibited arachidonate release induced by zymosan. They also inhibited the zymosan-induced formation of inositol phosphates, which hints that an inhibitory effect at the phospholipase C level might explain the inhibition of the response to zymosan. 4. Quinacrine, and to a lesser extent chloroquine, has an inhibitory effect on the lipopolysaccharide- or zymosan-induced expression of interleukin 1β and tumor necrosis factor α, both at the mRNA and protein levels. This, in particular, has important implications for the mode of action of these compounds in rheumatoid arthritis.</div></front></TEI><affiliations><list><country><li>Suède</li></country></list><tree><country name="Suède"><noRegion><name sortKey="Bondeson, Jan" sort="Bondeson, Jan" uniqKey="Bondeson J" first="Jan" last="Bondeson">Jan Bondeson</name></noRegion><name sortKey="Sundler, Roger" sort="Sundler, Roger" uniqKey="Sundler R" first="Roger" last="Sundler">Roger Sundler</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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