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花生四烯酸致炎小鼠耳中前列腺素和白三烯的合成

Prostaglandin and leukotriene synthesis in mouse ears inflamed by arachidonic acid.

作者信息

Opas E E, Bonney R J, Humes J L

出版信息

J Invest Dermatol. 1985 Apr;84(4):253-6. doi: 10.1111/1523-1747.ep12265320.

Abstract

Topical application of arachidonic acid on mouse ears induces the synthesis of prostaglandin E2 and leukotrienes C4 and D4. The increased tissue levels of these products are quantitated by radioimmunoassay. The identity of the leukotrienes was confirmed by immunoreactivity of reverse-phase high-performance liquid chromatography fractions corresponding to authentic standards. Synthesis of the arachidonic acid metabolites precedes or is coincident with increased vascular permeability resulting in an edematous response, as measured by accumulation of [125I]albumin in the ear after i.v. injection or by tissue wet weight. When applied topically, anti-inflammatory drugs such as BW755C (3-amino-1-(m-[trifluoromethyl]phenyl)2-pyrazoline, indomethacin, and nordihydroguaiaretic acid inhibit edema and modulate the appearance of the arachidonic acid products. The data suggest the coinvolvement of prostaglandin E2 and leukotrienes C4 and D4 as mediators of inflammation in this in vivo model.

摘要

将花生四烯酸局部应用于小鼠耳部可诱导前列腺素E2以及白三烯C4和D4的合成。这些产物组织水平的升高通过放射免疫测定法定量。通过与标准品对应的反相高效液相色谱馏分的免疫反应性来确认白三烯的同一性。花生四烯酸代谢产物的合成先于或与血管通透性增加同时发生,导致水肿反应,这可通过静脉注射后耳部[125I]白蛋白的积聚或组织湿重来测量。局部应用时,诸如BW755C(3-氨基-1-(间-[三氟甲基]苯基)2-吡唑啉)、吲哚美辛和去甲二氢愈创木酸等抗炎药物可抑制水肿并调节花生四烯酸产物的出现。数据表明,在这个体内模型中,前列腺素E2以及白三烯C4和D4作为炎症介质发挥作用。

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