Inhibition of histamine secretion from mast cells by disodium cromoglycate: an enigma still?

Pearce, F. L.

doi:10.1016/0165-6147(85)90182-8

Cited by 6 publications

(1 citation statement)

References 17 publications

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“…Although DSCG was introduced as an anti-asthmatic drug nearly twenty years ago, its precise mode of action still remains an enigma (Pearce, 1985). Classically, the drug is believed to stabilize the cell membrane of connective tissue mast cells, thus preventing the release of allergic mediators such as histamine or leukotrienes (Schwender, 1983;Tasaka, 1985).…”

Section: Introductionmentioning

confidence: 99%

Cytoprotective effects of disodium cromoglycate on rat stomach mucosa

Goossens

Reempts

Wauwe

1987

British J Pharmacology

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The cytoprotective effects of the anti‐asthmatic drug, disodium cromoglycate (DSCG), on gastric mucosal necrosis induced by ethanol in rats were studied. Subcutaneous, but not oral, DSCG prevented the formation of gastric lesions and this effect was dose‐dependent between 1.25 and 40 mg kg−1, with an ED50 value of 6.8 mg kg−1. Maximal cytoprotection occurred 15–30 min after DSCG treatment. Histological examination revealed that DSCG effectively protected the gastric mucosa against ethanol‐induced vascular congestion, haemorrhage, epithelial desquamation and mucosal oedema. Enhanced production of endogenous prostaglandins, which are known cytoprotective compounds, could not explain the mucosal protection. At a dose of 40 mg kg−1, DSCG did not change prostaglandin E2 or 6‐keto‐prostaglandin F1α concentrations in gastric mucosal tissue, although its cytoprotective activity was partially inhibited by prior treatment of the animals with indomethacin.

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Section: Introductionmentioning

confidence: 99%

Cytoprotective effects of disodium cromoglycate on rat stomach mucosa

Goossens

Reempts

Wauwe

1987

British J Pharmacology

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Differential inhibition by nedocromil sodium of superoxide generation elicited by platelet activating factor in human neutrophils

1990

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Nedocromil sodium (10(-10) - 10(-9) M) produced a dose-related inhibition of superoxide anion generation induced by platelet activating factor (PAF) in human polymorphonuclear leukocytes (PMNs). At a higher concentration (3 x 10(-7) M), nedocromil sodium significantly inhibited superoxide generation elicited by N-formyl-methionyl-leucylphenylalanine, but was unable to block the response to phorbol dibutyrate. Nedocromil sodium (10(-11) - 10(-5) M) enhanced PAF-stimulated lysozyme release in a non-concentration-dependent manner, and was completely ineffective in depressing PAF-induced release of [3H]arachidonic acid and the rise in cytosolic Ca2+. The preferential inhibitory effects of nedocromil sodium on PAF-induced activation of superoxide generation may provide insight into the therapeutic action of this drug as an anti-asthmatic agent.

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