Inhibition of Prostaglandin Biosynthesis by Corticosteroids

Greaves, Malcolm W.; McDonald-Gibson, Wendy J.

doi:10.1136/bmj.2.5805.83

Cited by 79 publications

(19 citation statements)

References 15 publications

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“…It is of particular interest to note that the two patients undergoing local steroid therapy at the time of sampling had little inflammation and negligible quantities of prostaglandin-like activity. It is possible that the steroids inhibited prostaglandin synthesis (Greaves and McDonald-Gibson, 1972), or they may just have suppressed the acute inflammatory process.…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin-like Activity in Ocular Inflammation

Eakins¹,

Whitelocke²,

Bennett³

et al. 1972

BMJ

130

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Section: Discussionmentioning

confidence: 99%

Prostaglandin-like Activity in Ocular Inflammation

Eakins¹,

Whitelocke²,

Bennett³

et al. 1972

BMJ

130

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“…irradiated guinea-pig skin. There is also evidence that corticosteroids may inhibit synthesis and the release of these substances (Greaves & McDonald-Gibson, 1972;Lewis & Piper, 1975). Propyl gallate at high concentration also inhibits prostaglandin formation (van Dorp, 1967) a factor which may contribute to its topical anti-erythemic efficacy.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Systemically and Topically Applied Drugs on Ultraviolet‐induced Erythema in the Rat

Law¹,

Lewis²

1977

British J Pharmacology

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Exposure of the skin of rats to u.v. light (>295 nm) for 30 s or longer elicited a delayed erythema response, the rate of onset increasing with the period of irradiation. The erythema was still present at 24 h and was replaced by scab formation in 48 hours. Both topically applied steroidal and non‐steroidal anti‐inflammatory drugs reduced the erythema formation when administered immediately after u.v. exposure. Propyl gallate, an antioxidant with sun screening properties in man, also possessed topical anti‐erythemic activity. Both steroidal and non‐steroidal anti‐inflammatory drugs, systemically administered 1 h before u.v. exposure, reduced the erythema. However, the steroidal compounds were less effective than the nonsteroids and reduced the intensity of erythema by less than 50%. Antagonists of 5‐hydroxytryptamine (5‐HT) reduced the erythema but several other drugs with different pharmacological activities were ineffective. Neither topical nor systemic treatments of any of the drugs examined suppressed the scab formation at 48 hours. These results and those using other selective blocking agents indicate that in the mediation of the erythema reaction prostaglandins may play a major role and 5‐HT perhaps a minor one but that H1 histamine receptors and α‐ and β‐adrenoceptors have no significant role.

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“…This effect has also been reported for newer nonsteroidal anti-inflammatory agents as well (10)(11)(12). Steroidal anti-inflammatory agents were found to reduce the amount of prostaglandin in inflamed rabbit eyes (13) and to inhibit synthesis of prostaglandin in skin (14). The anti-inflammatory corticoids also inhibit the uterotrophic response to estrogen (1 5-1 8).…”

mentioning

confidence: 57%