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MK886,一种强效且特异性的白三烯生物合成抑制剂,可阻断并逆转离子载体刺激的白细胞中5-脂氧合酶的膜结合。

MK886, a potent and specific leukotriene biosynthesis inhibitor blocks and reverses the membrane association of 5-lipoxygenase in ionophore-challenged leukocytes.

作者信息

Rouzer C A, Ford-Hutchinson A W, Morton H E, Gillard J W

机构信息

Department of Pharmacology, Merck Frosst Centre for Therapeutic Research, Pointe Claire-Dorval, Québec, Canada.

出版信息

J Biol Chem. 1990 Jan 25;265(3):1436-42.

PMID:2104841
Abstract

Recently, we have shown that ionophore activation of human leukocytes results in leukotriene synthesis and a translocation of 5-lipoxygenase from the cytosol to cellular membrane. This membrane translocation was postulated to be an important early activation step for the enzyme. 3-[1-(p-Chlorobenzyl)-5-(isopropyl)-3-tert-butylthioindol-2-yl]-2, 2- dimethylpropanoic acid (MK886) is a potent and specific inhibitor of leukotriene biosynthesis in vivo and in intact cells, but has no direct effect on 5-lipoxygenase activity in cell-free systems. In this report, we show that MK886 can both prevent and reverse the membrane translocation of 5-lipoxygenase, in conjunction with the inhibition of leukotriene synthesis. Similar compounds of the indole class could also inhibit the membrane translocation of 5-lipoxygenase in a rank order of potency that correlated with their potencies for leukotriene synthesis inhibition. In contrast L-656,224, a direct 5-lipoxygenase inhibitor, had no effect on the translocation of the enzyme. Attempts to demonstrate the effects of MK886 on the association of 5-lipoxygenase with membrane in cell-free preparations failed due to a nonspecific Ca2+-dependent sedimentation of the enzyme. The mechanism of action of MK-886 is therefore to block translocation, prevent subsequent activation of 5-lipoxygenase, and hence block cellular leukotriene biosynthesis.

摘要

最近,我们已经证明,离子载体激活人白细胞会导致白三烯合成以及5-脂氧合酶从胞质溶胶转位至细胞膜。这种膜转位被认为是该酶早期激活的一个重要步骤。3-[1-(对氯苄基)-5-(异丙基)-3-叔丁硫基吲哚-2-基]-2,2-二甲基丙酸(MK886)是体内和完整细胞中白三烯生物合成的一种强效且特异性抑制剂,但对无细胞体系中的5-脂氧合酶活性无直接影响。在本报告中,我们表明MK886既能预防又能逆转5-脂氧合酶的膜转位,同时抑制白三烯合成。吲哚类的类似化合物也能抑制5-脂氧合酶的膜转位,其效力顺序与它们抑制白三烯合成的效力相关。相比之下,直接的5-脂氧合酶抑制剂L-656,224对该酶的转位没有影响。由于该酶非特异性的Ca2+依赖性沉降,在无细胞制剂中尝试证明MK886对5-脂氧合酶与膜结合的影响未成功。因此,MK-886的作用机制是阻断转位,防止5-脂氧合酶随后的激活,从而阻断细胞白三烯生物合成。

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