The effect of anti-inflammatory agents on human synovial fibroblast prostaglandin synthetase
Identifieur interne : 003966 ( Main/Exploration ); précédent : 003965; suivant : 003967The effect of anti-inflammatory agents on human synovial fibroblast prostaglandin synthetase
Auteurs : David S. Newcombe [États-Unis] ; Yoshinori Ishikawa [États-Unis]Source :
- Prostaglandins [ 0090-6980 ] ; 1976.
English descriptors
- Teeft :
- Assay, Biosynthesis, Cofactor, Corticosteroid, Cyclic, Edta, Enzyme activity, Epinephrine, Fibroblast, Gold chloride, Human synovial fibroblasts, Hydrocortisone, Indomethacin, Inflammatory, Inhibitory effect, November, Particulate protein, Pgel, Phenylbutazone, Prostaglandin, Prostaglandin biosynthesis, Prostaglandin formation, Prostaglandin production, Prostaglandin synthesis, Prostaglandin synthetase, Prostaglandin synthetase activity, Reaction mixture, Rheumatoid, Rheumatoid arthritis, Rheumatoid synovia, Synovial, Synovial fibroblast prostaglandin synthetase activity, Synthetase.
Abstract
Abstract: Human synovial fibroblast prostaglandin synthetase activity is inhibited by many different non-steroidal anti-inflammatory agents. Aspirin, indomethacin and phenylbutazone significantly inhibit both PGE1, PGE2 and PGF1α and PGF2α synthesis; whereas penicillamine and aurothioglucose are more potent inhibitors of the F prostaglandins. Histidine and antimalarials do not inhibit, to a significant degree, human synovial prostaglandin synthetase activity. Hydrocortisone has no direct effect on prostaglandin synthetase activity. No changes in synthetase activity are observed when synovial cells are incubated with hydrocortisone, and the prostaglandin synthetase system subsequently isolated and assayed. The proposed inhibitory effects of hydrocortisone on prostaglandin production by synovium may be the result of an alteration of enzyme substrate or cofactor concentration rather than a direct effect on prostaglandin synthetase.
Url:
DOI: 10.1016/0090-6980(76)90059-9
Affiliations:
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Newcombe</name></author><author><name sortKey="Ishikawa, Yoshinori" sort="Ishikawa, Yoshinori" uniqKey="Ishikawa Y" first="Yoshinori" last="Ishikawa">Yoshinori Ishikawa</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:B4B6BF9C28033C61782A905EAD3C019776008A68</idno><date when="1976" year="1976">1976</date><idno type="doi">10.1016/0090-6980(76)90059-9</idno><idno type="url">https://api.istex.fr/ark:/67375/6H6-P6J0VZN5-N/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">002723</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">002723</idno><idno type="wicri:Area/Istex/Curation">002723</idno><idno type="wicri:Area/Istex/Checkpoint">002713</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Checkpoint">002713</idno><idno type="wicri:doubleKey">0090-6980:1976:Newcombe D:the:effect:of</idno><idno type="wicri:Area/Main/Merge">003A45</idno><idno type="wicri:Area/Main/Curation">003966</idno><idno type="wicri:Area/Main/Exploration">003966</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">The effect of anti-inflammatory agents on human synovial fibroblast prostaglandin synthetase</title><author><name sortKey="Newcombe, David S" sort="Newcombe, David S" uniqKey="Newcombe D" first="David S." last="Newcombe">David S. Newcombe</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Vermont</region></placeName><wicri:cityArea>Division of Rheumatology, Department of Medicine, University of Vermont, College of Medicine, Burlington</wicri:cityArea></affiliation></author><author><name sortKey="Ishikawa, Yoshinori" sort="Ishikawa, Yoshinori" uniqKey="Ishikawa Y" first="Yoshinori" last="Ishikawa">Yoshinori Ishikawa</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Vermont</region></placeName><wicri:cityArea>Division of Rheumatology, Department of Medicine, University of Vermont, College of Medicine, Burlington</wicri:cityArea></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="1976">1976</date><biblScope unit="volume">12</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="849">849</biblScope><biblScope unit="page" to="869">869</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>Assay</term><term>Biosynthesis</term><term>Cofactor</term><term>Corticosteroid</term><term>Cyclic</term><term>Edta</term><term>Enzyme activity</term><term>Epinephrine</term><term>Fibroblast</term><term>Gold chloride</term><term>Human synovial fibroblasts</term><term>Hydrocortisone</term><term>Indomethacin</term><term>Inflammatory</term><term>Inhibitory effect</term><term>November</term><term>Particulate protein</term><term>Pgel</term><term>Phenylbutazone</term><term>Prostaglandin</term><term>Prostaglandin biosynthesis</term><term>Prostaglandin formation</term><term>Prostaglandin production</term><term>Prostaglandin synthesis</term><term>Prostaglandin synthetase</term><term>Prostaglandin synthetase activity</term><term>Reaction mixture</term><term>Rheumatoid</term><term>Rheumatoid arthritis</term><term>Rheumatoid synovia</term><term>Synovial</term><term>Synovial fibroblast prostaglandin synthetase activity</term><term>Synthetase</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Human synovial fibroblast prostaglandin synthetase activity is inhibited by many different non-steroidal anti-inflammatory agents. Aspirin, indomethacin and phenylbutazone significantly inhibit both PGE1, PGE2 and PGF1α and PGF2α synthesis; whereas penicillamine and aurothioglucose are more potent inhibitors of the F prostaglandins. Histidine and antimalarials do not inhibit, to a significant degree, human synovial prostaglandin synthetase activity. Hydrocortisone has no direct effect on prostaglandin synthetase activity. No changes in synthetase activity are observed when synovial cells are incubated with hydrocortisone, and the prostaglandin synthetase system subsequently isolated and assayed. The proposed inhibitory effects of hydrocortisone on prostaglandin production by synovium may be the result of an alteration of enzyme substrate or cofactor concentration rather than a direct effect on prostaglandin synthetase.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Vermont</li></region></list><tree><country name="États-Unis"><region name="Vermont"><name sortKey="Newcombe, David S" sort="Newcombe, David S" uniqKey="Newcombe D" first="David S." last="Newcombe">David S. Newcombe</name></region><name sortKey="Ishikawa, Yoshinori" sort="Ishikawa, Yoshinori" uniqKey="Ishikawa Y" first="Yoshinori" last="Ishikawa">Yoshinori Ishikawa</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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