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硝基血管扩张剂诱导的人中性粒细胞白三烯B4释放的抑制作用可能由环鸟苷酸介导。

Nitrovasodilator-induced inhibition of LTB4 release from human PMN may be mediated by cyclic GMP.

作者信息

Ney P, Schröder H, Schrör K

机构信息

Institut für Pharmakologie, Heinrich-Heine-Universität Düsseldorf, Federal Republic of Germany.

出版信息

Eicosanoids. 1990;3(4):243-5.

PMID:1963541
Abstract

This study investigates the action of nitrovasodilators on f-metleu-phe (FMLP)-stimulated LTB4 release and intracellular cyclic nucleotide levels in human polymorphonuclear leukocytes (PMN). Sodium nitroprusside, and the molsidomine (MOL) metabolites SIN-1 and SIN-1A potently inhibited LTB4 release and increased cGMP levels. No significant effects on LTB4 release or cGMP accumulation were observed in the presence of molsidomine or glyceryl trinitrate. None of the compounds tested affected cAMP levels. It is suggested that nitrovasodilators (i) inhibit LTB4 release from human PMN via enhanced cGMP and (ii) that this inhibition requires the presence of an active metabolite, probably nitric oxide.

摘要

本研究调查了硝血管扩张剂对人多形核白细胞(PMN)中f-甲硫氨酰-亮氨酰-苯丙氨酸(FMLP)刺激的白三烯B4(LTB4)释放及细胞内环核苷酸水平的作用。硝普钠以及吗多明(MOL)的代谢产物SIN-1和SIN-1A能有效抑制LTB4释放并提高环鸟苷酸(cGMP)水平。在吗多明或硝酸甘油存在的情况下,未观察到对LTB4释放或cGMP积累有显著影响。所测试的化合物均未影响环磷酸腺苷(cAMP)水平。研究表明,硝血管扩张剂(i)通过增强cGMP抑制人PMN释放LTB4,且(ii)这种抑制作用需要活性代谢产物的存在,可能是一氧化氮。

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