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白三烯C4参与血小板活化因子诱导的小鼠死亡。

Involvement of leukotriene C4 in PAF-induced death in mice.

作者信息

Tsunoda H, Abe S, Sakuma Y, Katayama S, Katayama K

机构信息

Inflammation and Allergy Research Unit, Eisai Research Laboratories, Ibaraki, Japan.

出版信息

Prostaglandins Leukot Essent Fatty Acids. 1990 Apr;39(4):291-4. doi: 10.1016/0952-3278(90)90008-9.

DOI:10.1016/0952-3278(90)90008-9
PMID:2353029
Abstract

The role of leukotrienes (LTs) in the pathogenesis of platelet-activating factor (PAF)-induced death in mice was reinvestigated, since previously reported results are in conflict. A novel 5-lipoxygenase inhibitor, E6080, and a leukotriene antagonist, LY17883, protected mice from PAF-induced death in a dose-dependent manner, while the well-known 5-lipoxygenase inhibitor, AA861, was less effective than E6080. After the intravenous injection of PAF in mice, immunoreactive leukotriene C4 (i-LTC4), which was co-eluted with authentic LTC4 in HPLC, was significantly increased in bronchoalveolar lavage fluid (BALF). Oral administration of E6080 suppressed the increase in i-LTCM4. The results suggest that LTs may play an important role in PAF-induced lethality in mice.

摘要

鉴于先前报道的结果相互矛盾,对白三烯(LTs)在血小板活化因子(PAF)诱导的小鼠死亡发病机制中的作用进行了重新研究。一种新型5-脂氧合酶抑制剂E6080和一种白三烯拮抗剂LY17883以剂量依赖性方式保护小鼠免受PAF诱导的死亡,而著名的5-脂氧合酶抑制剂AA861的效果不如E6080。给小鼠静脉注射PAF后,支气管肺泡灌洗液(BALF)中与真实LTC4在高效液相色谱中共洗脱的免疫反应性白三烯C4(i-LTC4)显著增加。口服E6080可抑制i-LTC4的增加。结果表明,LTs可能在PAF诱导的小鼠致死性中起重要作用。

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引用本文的文献

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CGS 26529: the biological profile of a novel, orally active 5-lipoxygenase inhibitor with an extended duration of action.CGS 26529:一种新型口服活性5-脂氧合酶抑制剂的生物学特性,作用持续时间延长。
Inflamm Res. 1995 Aug;44 Suppl 2:S147-8. doi: 10.1007/BF01778305.