Source of endogenous arachidonate and 5-lipoxygenase products in human neutrophils stimulated by bradykinin and A23187.
作者： O H Nielsen , K Bukhave , I Ahnfelt-Ronne , J Rask-Madsen
DOI: 10.1136/GUT.29.3.319
关键词:
摘要: The lipoxygenase products of arachidonic acid (AA) metabolism, 5-hydroxyeicosatetraenoic (5-HETE) and leucotriene B4 (LTB4), are considered to have an important pathophysiological role in inflammatory bowel disease by stimulating the response contributing diarrhoea. present studies were designed investigate effect physiological stimulants bradykinin (BK) 5-hydroxytryptamine (5-HT), addition influence calcium ionophore A23187, on source AA release 5-lipoxygenation human neutrophils (PMNs) vitro. This was done elucidate specificity mechanism which PMNs respond physiological, extracellular Ca2+ dependent agonists. results study indicate that stimulation 1-14C-AA-prelabelled with BK liberates mainly from phosphatidylinositol, while A23187 causes phosphatidylcholine, phosphatidylethanolamine, possibly phosphatidylserine. Furthermore (10(-9)-10(-6)M) dose-dependently stimulated formation 5-HETE LTB4, reaching a maximum at 10(-7)M, 5-HT (10(-8)-10(-4)M) released only negligible amounts eicosanoids, similar those observed control experiments. Stimulation (10(-5)M) caused high both LTB4. These offer evidence BK, but not 5-HT, initiates binding specific receptors external surface PMNs, whereas accelerates through mechanisms do involve cell receptor.
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