Mechanism of cyclosporin A-induced inhibition of prostacyclin synthesis by macrophages
Identifieur interne : 002240 ( Istex/Checkpoint ); précédent : 002239; suivant : 002241Mechanism 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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ISTEX:CB30EED0C8DAA24D12119EB0E2FB621DAB666221Le document en format XML
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<term>Cyclosporin</term>
<term>Dexamethasone</term>
<term>Drug concentration</term>
<term>Exogenous arachidonic acid</term>
<term>Glucocorticoid</term>
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<term>Increase membrane</term>
<term>Indomethacin</term>
<term>Macrophage</term>
<term>Membrane phospholipids</term>
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<term>November</term>
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<term>Present study</term>
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<term>Prostaglandin formation</term>
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<term>Prostanoid production</term>
<term>Prostanoid synthesis</term>
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<term>Serumopsonized zymosan</term>
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<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>
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