Prostaglandin e production by cultured inflamed rat synovium; stimulation by colchicine and inhibition by chloroquine
Identifieur interne : 003902 ( Main/Exploration ); précédent : 003901; suivant : 003903Prostaglandin e production by cultured inflamed rat synovium; stimulation by colchicine and inhibition by chloroquine
Auteurs : Yizhar Floman [Israël]Source :
- Prostaglandines and Medicine [ 0161-4630 ] ; 1978.
English descriptors
- Teeft :
- Arachidonic, Arachidonic acid, Arthritis, Chloroquine, Chloroquine diphosphate, Colchicine, Experimental arthritis, Floman, Incubation, Incubation medium, Inflamed, Inflamed synovium, Inflammation, Polymorphonuclear leucocytes, Present investigation, Prostaglandin, Prostaglandin biosynthesis, Prostaglandin production, Prostaglandin synthesis, Prostaglandin synthetase inhibitors, Raven press, Rheumatoid, Rheumatoid arthritis, Steroid, Substrate availability, Synovium, Synthetase, Tissue content, Vane.
Abstract
Abstract: Acute arthritis was induced by injection of cell-free extract of group A type 4 Streptococci, into the knee joints of three month old male rats. Slices of the inflamed synovium obtained from these rats were incubated for 60–240 minutes, and the rate of prostaglandin E accumulation in the medium was measured by radioimmunoassay.Prostaglandins of the E type accumulated in the medium at a near linear rate during the incubation of the inflamed synovium for 4 hours. Incubation of inflamed synovium in the presence of colchicine (10 μg/ml) brought about a two-fold increase in the prostaglandin E accumulation in the medium after a latency of one hour. Tissue content of prostaglandin E after 4 hours of incubation of inflamed synovium with colchicine doubled as well. In contrast, incubation of inflamed synovium with chloroquine (10 μg/ml), corticosterone or dexamethasone (100 μg/ml each) reduced prostaglandin E accumulation in the medium by 50% at 1–4 hours. Likewise, chloroquine, corticosterone or dexamethasone reduced the tissue content of prostaglandin E in the inflamed synovium after 4 hours of incubation. The suppressive action of chloroquine was prevented by addition to the medium of arachidonic acid (2 μg/ml).It is concluded that the anti-inflammatory properties of colchicine are probably not related to prostaglandin biosynthesis. On the other hand chloroquine exerts its anti-inflammatory properties by curtailing substrate availability (arachidonic acid) for prostaglandin production, similarly to the anti-inflammatory mechanism of steroid hormones.
Url:
DOI: 10.1016/0161-4630(78)90075-7
Affiliations:
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Le document en format XML
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<term>Chloroquine diphosphate</term>
<term>Colchicine</term>
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<term>Rheumatoid arthritis</term>
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<term>Synovium</term>
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<front><div type="abstract" xml:lang="en">Abstract: Acute arthritis was induced by injection of cell-free extract of group A type 4 Streptococci, into the knee joints of three month old male rats. Slices of the inflamed synovium obtained from these rats were incubated for 60–240 minutes, and the rate of prostaglandin E accumulation in the medium was measured by radioimmunoassay.Prostaglandins of the E type accumulated in the medium at a near linear rate during the incubation of the inflamed synovium for 4 hours. Incubation of inflamed synovium in the presence of colchicine (10 μg/ml) brought about a two-fold increase in the prostaglandin E accumulation in the medium after a latency of one hour. Tissue content of prostaglandin E after 4 hours of incubation of inflamed synovium with colchicine doubled as well. In contrast, incubation of inflamed synovium with chloroquine (10 μg/ml), corticosterone or dexamethasone (100 μg/ml each) reduced prostaglandin E accumulation in the medium by 50% at 1–4 hours. Likewise, chloroquine, corticosterone or dexamethasone reduced the tissue content of prostaglandin E in the inflamed synovium after 4 hours of incubation. The suppressive action of chloroquine was prevented by addition to the medium of arachidonic acid (2 μg/ml).It is concluded that the anti-inflammatory properties of colchicine are probably not related to prostaglandin biosynthesis. On the other hand chloroquine exerts its anti-inflammatory properties by curtailing substrate availability (arachidonic acid) for prostaglandin production, similarly to the anti-inflammatory mechanism of steroid hormones.</div>
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