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Prostaglandin e production by cultured inflamed rat synovium; stimulation by colchicine and inhibition by chloroquine

Identifieur interne : 003902 ( Main/Exploration ); précédent : 003901; suivant : 003903

Prostaglandin e production by cultured inflamed rat synovium; stimulation by colchicine and inhibition by chloroquine

Auteurs : Yizhar Floman [Israël]

Source :

RBID : ISTEX:ED8E4381F38EACE3BF728E0005D7705844F0248E

English descriptors

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</term>
<term>Chloroquine diphosphate</term>
<term>Colchicine</term>
<term>Experimental arthritis</term>
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<term>Prostaglandin production</term>
<term>Prostaglandin synthesis</term>
<term>Prostaglandin synthetase inhibitors</term>
<term>Raven press</term>
<term>Rheumatoid</term>
<term>Rheumatoid arthritis</term>
<term>Steroid</term>
<term>Substrate availability</term>
<term>Synovium</term>
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<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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