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乙胺嗪可减轻乙醇对大鼠胃黏膜的损伤。

Diethylcarbamazine decreases ethanol-injury to the gastric mucosa of the rat.

作者信息

Balaa M A, Subramony C

机构信息

Good Samaritan Medical Groups, San Jose, CA 94124.

出版信息

Eicosanoids. 1990;3(4):201-3.

PMID:2127366
Abstract

Exposure of the rat stomach to ethanol stimulates the generation of leukotrienes. Leukotrienes are potent mediators of tissue inflammation and injury. In this work we show that pretreatment with diethylcarbamazine, a lipoxygenase enzyme inhibitor, significantly decreases ethanol injury to the rat gastric mucosa. At a dose of 250 mg/kg the compound significantly reduced the ETOH-stimulated mucosal LTC4 generation by 40% and PGE2 generation by 79%. We conclude that diethylcarbamazine is an inhibitor of the cyclooxygenase and lipoxygenase enzymes in the gastric mucosa. That inhibition of leukotriene synthesis decreases the extent of ethanol-stimulated suggests that leukotrienes play a key role in mediating ethanol-injury to that tissue.

摘要

将大鼠胃部暴露于乙醇中会刺激白三烯的生成。白三烯是组织炎症和损伤的强效介质。在本研究中,我们发现用脂氧合酶抑制剂乙胺嗪进行预处理可显著降低乙醇对大鼠胃黏膜的损伤。在250mg/kg的剂量下,该化合物可使乙醇刺激的黏膜LTC4生成显著减少40%,PGE2生成减少79%。我们得出结论,乙胺嗪是胃黏膜中环氧化酶和脂氧合酶的抑制剂。对白三烯合成的抑制降低了乙醇刺激的程度,这表明白三烯在介导乙醇对该组织的损伤中起关键作用。

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