Mechanism of cyclosporin A-induced inhibition of prostacyclin synthesis by macrophages
Identifieur interne : 003482 ( Main/Exploration ); précédent : 003481; suivant : 003483Mechanism of cyclosporin A-induced inhibition of prostacyclin synthesis by macrophages
Auteurs : T.-P. D. Fan ; G. P. LewisSource :
- Prostaglandins [ 0090-6980 ] ; 1985.
English descriptors
- Teeft :
- Absolute ethanol, Arachidonic, Arachidonic acid, Basal level, Culture medium, Cyclosporin, Dexamethasone, Drug concentration, Exogenous arachidonic acid, Glucocorticoid, Graft rejection, Increase membrane, Indomethacin, Macrophage, Membrane phospholipids, Mononuclear cells, November, Peritoneal, Peritoneal macrophages, Phospholipase, Present experiments, Present investigation, Present study, Prostaglandin, Prostaglandin formation, Prostanoid, Prostanoid production, Prostanoid synthesis, Separate experiments, Serumopsonized zymosan, Skin grafts, Zymosan.
Abstract
Abstract: In vitro studies of PG production over a 24 h period by adherent rat peritoneal macrophages activated by serum-opsonized zymosan revealed that CSA (0.3 – 10 μg/ml) caused a dose-related inhibition of PGI2 (assayed as 6-oxo-PGF1α) formation. Indomethacin (IND, 0.01 – 10 μg/ml) and dexamethasone (DEX, 0.01 – 10 μg/ml) also inhibited the PG production in a dose-related manner. When arachidonic acid (10 μg/ml) was added together with the inhibitors, there was no change in the level of PGI2 produced by IND-treated cells whilst the PGI2 levels of DEX- and CSA-treated cells were elevated to the control level. Therefore CSA like DEX does not inhibit cyclo-oxygenase activity. However unlike DEX, CSA (1 – 30 μg/ml) caused inhibition of phospholipase A2 (PLA2) activity when assayed on the hydrolysis of a synthetic substrate by pancreatic PLA2 in a cell-free system. The direct inhibition of PLA2 might well be a manifestation of the fundamental activity of CSA on immunocompetent cells.
Url:
DOI: 10.1016/0090-6980(85)90004-8
Affiliations:
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D." last="Fan">T.-P. D. Fan</name><affiliation><wicri:noCountry code="no comma">Department of Pharmacology Institute of Basic Medical Sciences Royal College of Surgeons of England London WC2A 3PN UK</wicri:noCountry></affiliation></author><author><name sortKey="Lewis, G P" sort="Lewis, G P" uniqKey="Lewis G" first="G. P." last="Lewis">G. P. Lewis</name><affiliation><wicri:noCountry code="no comma">Department of Pharmacology Institute of Basic Medical Sciences Royal College of Surgeons of England London WC2A 3PN UK</wicri:noCountry></affiliation></author></analytic><monogr></monogr><series><title level="j">Prostaglandins</title><title level="j" type="abbrev">PROOLD</title><idno type="ISSN">0090-6980</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1985">1985</date><biblScope unit="volume">30</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="735">735</biblScope><biblScope unit="page" to="747">747</biblScope></imprint><idno type="ISSN">0090-6980</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0090-6980</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Absolute ethanol</term><term>Arachidonic</term><term>Arachidonic acid</term><term>Basal level</term><term>Culture medium</term><term>Cyclosporin</term><term>Dexamethasone</term><term>Drug concentration</term><term>Exogenous arachidonic acid</term><term>Glucocorticoid</term><term>Graft rejection</term><term>Increase membrane</term><term>Indomethacin</term><term>Macrophage</term><term>Membrane phospholipids</term><term>Mononuclear cells</term><term>November</term><term>Peritoneal</term><term>Peritoneal macrophages</term><term>Phospholipase</term><term>Present experiments</term><term>Present investigation</term><term>Present study</term><term>Prostaglandin</term><term>Prostaglandin formation</term><term>Prostanoid</term><term>Prostanoid production</term><term>Prostanoid synthesis</term><term>Separate experiments</term><term>Serumopsonized zymosan</term><term>Skin grafts</term><term>Zymosan</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: In vitro studies of PG production over a 24 h period by adherent rat peritoneal macrophages activated by serum-opsonized zymosan revealed that CSA (0.3 – 10 μg/ml) caused a dose-related inhibition of PGI2 (assayed as 6-oxo-PGF1α) formation. Indomethacin (IND, 0.01 – 10 μg/ml) and dexamethasone (DEX, 0.01 – 10 μg/ml) also inhibited the PG production in a dose-related manner. When arachidonic acid (10 μg/ml) was added together with the inhibitors, there was no change in the level of PGI2 produced by IND-treated cells whilst the PGI2 levels of DEX- and CSA-treated cells were elevated to the control level. Therefore CSA like DEX does not inhibit cyclo-oxygenase activity. However unlike DEX, CSA (1 – 30 μg/ml) caused inhibition of phospholipase A2 (PLA2) activity when assayed on the hydrolysis of a synthetic substrate by pancreatic PLA2 in a cell-free system. The direct inhibition of PLA2 might well be a manifestation of the fundamental activity of CSA on immunocompetent cells.</div></front></TEI><affiliations><list></list><tree><noCountry><name sortKey="Fan, T P D" sort="Fan, T P D" uniqKey="Fan T" first="T.-P. D." last="Fan">T.-P. D. Fan</name><name sortKey="Lewis, G P" sort="Lewis, G P" uniqKey="Lewis G" first="G. P." last="Lewis">G. P. Lewis</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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