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过敏反应的前列腺素生成因子可诱导人呼吸道释放黏液糖蛋白并形成花生四烯酸的脂氧合酶产物。

Prostaglandin-generating factor of anaphylaxis induces mucous glycoprotein release and the formation of lipoxygenase products of arachidonate from human airways.

作者信息

Marom Z, Shelhamer J H, Steel L, Goetzl E J, Kaliner M

出版信息

Prostaglandins. 1984 Jul;28(1):79-91. doi: 10.1016/0090-6980(84)90115-1.

Abstract

The effects of prostaglandin-generating factor of anaphylaxis (PGF-A) upon the lipoxygenation of arachidonic acid and the promotion of mucous glycoprotein secretion by human airways were analyzed concurrently in order to determine the role that lipoxygenase products play in the secretion of mucus which accompanies immediate hypersensitivity reactions of airways. PGF-A enhanced both mucous glycoprotein release and the 5- and 15-lipoxygenation of arachidonic acid as well as the formation of leukotriene B4 (LTB4) with similar dose-response relationships. The capacity of PGF-A to stimulate mucous glycoprotein release was inhibited by ETYA but not by indomethacin, suggesting that PGF-A stimulated lipoxygenase products may be involved. Lipoxygenase products of arachidonic acid thus may serve as mediators of the enhancement of mucus secretion from human airways in response to PGF-A.

摘要

同时分析了过敏反应中前列腺素生成因子(PGF-A)对花生四烯酸脂氧化作用以及对人呼吸道黏液糖蛋白分泌促进作用的影响,以确定脂氧合酶产物在伴随呼吸道速发型超敏反应的黏液分泌中所起的作用。PGF-A增强了黏液糖蛋白释放、花生四烯酸的5-和15-脂氧化作用以及白三烯B4(LTB4)的形成,且具有相似的剂量反应关系。ETYA可抑制PGF-A刺激黏液糖蛋白释放的能力,但吲哚美辛无此作用,这表明PGF-A刺激产生的脂氧合酶产物可能参与其中。因此,花生四烯酸的脂氧合酶产物可能作为介质,介导人呼吸道黏液分泌因PGF-A而增强。

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