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人支气管肺泡灌洗细胞产生花生四烯酸和亚油酸代谢物。

Production of arachidonic acid and linoleic acid metabolites by human bronchoalveolar lavage cells.

作者信息

Engels F, Kessels G C, Schreurs A J, Nijkamp F P

机构信息

Department of Pharmacology, Faculty of Pharmacy, University of Utrecht, The Netherlands.

出版信息

Prostaglandins. 1991 Nov;42(5):441-50. doi: 10.1016/0090-6980(91)90035-e.

Abstract

Fatty acid-derived inflammatory mediators are considered to play an important role in airway hyperresponsiveness of asthmatic patients. The pulmonary macrophage may be an important source for these mediators in airway tissue. We investigated the metabolism of arachidonic acid and linoleic acid by human bronchoalveolar lavage cells, mainly comprising pulmonary macrophages. Arachidonic was mainly metabolized by 5-lipoxygenase, giving rise to the formation of leukotriene B4 and 5-hydroxy-eicosatetraenoic acid (5-HETE). Linoleic acid was converted to 5 major metabolites, including the 9-hydroxy and 13-hydroxy derivatives, 9- and 13-hydroxy-octadecadienoic acid (9- and 13-HODE). The formation of HODEs could be inhibited by cyclooxygenase inhibitors as well as lipoxygenase inhibitors, indicating that both enzymic species play a role in the generation of HODEs.

摘要

脂肪酸衍生的炎症介质被认为在哮喘患者的气道高反应性中起重要作用。肺巨噬细胞可能是气道组织中这些介质的重要来源。我们研究了主要由肺巨噬细胞组成的人支气管肺泡灌洗细胞对花生四烯酸和亚油酸的代谢。花生四烯酸主要通过5-脂氧合酶代谢,产生白三烯B4和5-羟基-二十碳四烯酸(5-HETE)。亚油酸转化为5种主要代谢产物,包括9-羟基和13-羟基衍生物,9-和13-羟基-十八碳二烯酸(9-和13-HODE)。环氧化酶抑制剂和脂氧合酶抑制剂均可抑制HODEs的形成,表明这两种酶在HODEs的生成中均起作用。

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