Corticosteroids inhibit prostaglandin production by rheumatoid synovia

Kantrowitz, Fred G.; Robinson, Dwight R.; McGuire, Mary B.; Levine, Lawrence

doi:10.1038/258737a0

Cited by 243 publications

(67 citation statements)

References 13 publications

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“…Corticosteroids have been reported to produce no inhibition of prostaglandin biosynthesis (Vane, 1971;Smith & Willis, 1971;Ferreira, Moncada & Vane, 1971), small degrees of inhibition at high concentrations (Greaves & McDonald-Gibson, 1972a & b) or marked inhibition at therapeutic concentrations (Lewis & Piper, 1975;Gryglewski, 1975;Kantrowitz et al, 1975b;Tashjian, Voelkel, McDonough & Levine, 1975) depending on the prostaglandin synthesizing preparation used. Prostaglandin production by cultured macrophages has been shown in this study to be inhibited by seven anti-inflammatory steroid preparations, with complete inhibition again being achieved at concentrations attained during antiinflammatory therapy in man.…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin Production by Macrophages and the Effect of Anti‐inflammatory Drugs

Bray¹,

Gordon

1978

British J Pharmacology

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Macrophages derived from peritoneal cavity inflammatory exudates of guinea‐pigs produced substantial amounts of prostaglandin E2‐like activity during in vitro culture, so providing the basis for an experimental model of prostaglandin production during inflammatory reactions. Dose‐related inhibition of prostaglandin biosynthesis was demonstrated by 16 acidic non‐steroidal anti‐inflammatory drugs. Seven anti‐inflammatory glucocorticosteroid preparations inhibited prostaglandin production in a dose‐related manner. The relative potencies of dexamethasone, prednisolone and hydrocortisone were consistent with clinical anti‐inflammatory ranking. Cortisone, however, failed to inhibit macrophage prostaglandin production. Three other agents used in the treatment of inflammatory joint diseases were examined. Sodium aurothiomalate inhibited prostaglandin production, although higher concentrations were toxic to macrophages. D‐Penicillamine did not affect macrophage prostaglandin production. Colchicine, in contrast, enhanced prostaglandin production at some concentrations. The probable significance of macrophages as a source of prostaglandins, during inflammatory responses, is discussed.

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Section: Discussionmentioning

confidence: 99%

Prostaglandin Production by Macrophages and the Effect of Anti‐inflammatory Drugs

Bray¹,

Gordon

1978

British J Pharmacology

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“…Initial studies, which used cell-free systems, failed to demonstrate any effect of antiinflammatory steroids on PG production (1,3,4). Recently, however, evidence was obtained that glucocorticoids decrease PG production in different in vitro systems via inhibition ofphospholipase activity (5)(6)(7)(8)(9)(10)(11)(12)(13). Although this action of glucocorticoids seems to be fairly reproducible in in vitro systems, especially with high doses of steroids, almost no data are available on the effect of glucocorticoids on PG synthesis in vivo.…”

Section: Introductionmentioning

confidence: 99%

Effect of dexamethasone on in vivo prostanoid production in the rabbit.

Náray-Fejes-Tóth¹,

Fejes-Tóth²,

Fischer³

et al. 1984

J. Clin. Invest.

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Abstract. To investigate the effects of antiinflammatory steroids on in vivo prostaglandin production, urinary excretion rates of six different cyclo-oxygenase products were determined before, during, and after the administration of dexamethasone (1 mg/kg per d). Urine was collected in metabolism cages and was analyzed for prostaglandins E2 and F2a (PGE2 and PGF2a,) by radioimmunoassay after open-column chromatography; 6-ketoprostaglandin Fla (6-keto-PGFIa) and thromboxane B2 (TxB2) were determined by radioimmunoassay after organic solvent extraction and reversed-phase high performance liquid chromatography; 7a-hydroxy-5,1 1-diketo-tetranorprostane-1,16-dioic acid (PGE-M) and 5a,7a-dihydroxy-11 -keto-tetranorprostane-1,16-dioicacid (PGF-M), the major urinary metabolites of prostaglandins E and F, were determined by gas chromatography-mass spectrometry and by radioimmunoassay, respectively. Dexamethasone failed to cause a statistically significant change in the excretion rate of PGE2 (control, 250.4±40.8; dexamethasone, 297.6±78.7 ng/kg per d).In contrast, PGF2, excretion decreased during administration of dexamethasone (from 1,036±228 to 449±158 ng/kg per d; P < 0.05). The urinary excretion rates of 6-keto-PGFia, TxB2, PGE-M, and PGF-M were not significantly altered by dexamethasone. (Control and dexamethasone values were, respectively, 63.6±7.9 and 103.5±17.9 ng/kg per d for 6-keto-PGFIa; 13.0±3.0 and 14.8±2.1 ng/kgperd for TxB2; 1,251+217 and 1,905±573 ng/kg per d for PGE-M; and 4,131±611 and 4,793±600 ng/kg per d for PGF-M.) Urine flow was significantly higher during dexamethasone administration (control, 159±24; dexamethasone, 305±29 ml/24 h; P < 0.01). However, no correlation could be detected between

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“…It has been demonstrated that the steroids exert anti inflammatory effects by preventing the release of arachidonic acid from phospholipids with resultant decrease in the production of prostaglandins and leucotrienes (1)(2)(3)(4)(5) Cutaneous reaction by autacoids and enzymes: In groups of 5 rats, each animal was given intradermally the following substances in 0.1 ml saline at different sites on the back: histamine, 50 /lg/ml; serotonin, 10 /ig/ml; trypsin, 50 /tg/ml; hyaluronidase, 250 TRU/ ml. Immediately following this, 1 ml of saline containing 2.5 mg Evans blue was injected i.v.…”

Section: Glucocorticoidsmentioning

confidence: 99%

Anti-allergic action of glucocorticoids in rats.

et al. 1983

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Abstract-The effects of three glucocorticoids (steroids: hydrocortisone, prednisolone and dexamethasone)on IgE antibody-mediated immediate hypersensitivity reactions in rats were studied.Forty-eight hr homologous passive cutaneous anaphylaxis (PCA) was inhibited in a dose response manner by the administration of steroids 2 hr prior to challenge.When steroids were administered at various times before challenge, each steroid showed different patterns of time courses for inhibition of homologous PCA. Maximum inhibition was obtained 2 hr after the administration of each steroid. The IgE antibody-mediated histamine release from peritoneal mast cells in vivo was inhibited by the administration of steroids. Time-courses for the inhibitory effects of steroids on histamine release were slightly different from those in PCA. The increase of capillary permeability caused by histamine, serotonin, trypsin or hyaluronidase in the rat skin was not affected by steroids.The inhibitory action of steroids on PCA was not influenced by non-corticoidal steroids (17a-methyltestosterone, androstenedione and progesterone) or arachidonic acid. These results partially explain the inhibitory action of steroids on IgE antibody-mediated immediate hypersensitivity.

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Corticosteroids inhibit prostaglandin production by rheumatoid synovia

Cited by 243 publications

References 13 publications

Prostaglandin Production by Macrophages and the Effect of Anti‐inflammatory Drugs

Prostaglandin Production by Macrophages and the Effect of Anti‐inflammatory Drugs

Effect of dexamethasone on in vivo prostanoid production in the rabbit.

Anti-allergic action of glucocorticoids in rats.

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