Flament J, Schandene L, Boeynaems J M
Department of Immunology, Erasme Hospital, Bruxelles.
Prostaglandins Leukot Essent Fatty Acids. 1988 Dec;34(3):175-80. doi: 10.1016/0952-3278(88)90142-1.
The effect of 6,9-deepoxy-6,9-(phenylimino)-delta 6,8-prostaglandin I1 (Piriprost) on the oxidative response was studied in human neutrophils stimulated by N-formyl-methionyl-leucyl-phenylalanine (fMLP), phorbol 12-myristate, 13-acetate (PMA) or opsonized zymosan. Piriprost inhibited the stimulatory effect of fMLP on superoxide anion (O2-) generation, at concentrations higher than those which depress leukotriene B4 (LTB4) formation. This inhibition was overcome by increasing the concentration of fMLP. Neither exogenous LTB4 nor indomethacin were able to reverse the inhibitory effect of piriprost on fMLP action. In contrast, piriprost did not inhibit the stimulation of O2- production induced by PMA or zymosan. Piriprost behaves thus as a specific and apparently competitive antagonist of fMLP: this action does not seem to involve lipoxygenase inhibition and might be exerted at the level of the fMLP receptor or its associated mechanisms of transduction.
研究了6,9-二环氧-6,9-（苯基亚氨基）-δ6,8-前列环素I1（匹立前列素）对由N-甲酰甲硫氨酰亮氨酰苯丙氨酸（fMLP）、佛波醇12-肉豆蔻酸酯13-乙酸酯（PMA）或调理酵母聚糖刺激的人中性粒细胞氧化反应的影响。匹立前列素在高于抑制白三烯B4（LTB4）形成的浓度时，抑制fMLP对超氧阴离子（O2-）生成的刺激作用。通过增加fMLP的浓度可克服这种抑制作用。外源性LTB4和吲哚美辛均不能逆转匹立前列素对fMLP作用的抑制效果。相反，匹立前列素不抑制由PMA或酵母聚糖诱导的O2-产生的刺激作用。因此，匹立前列素表现为fMLP的特异性且明显具有竞争性的拮抗剂：这种作用似乎不涉及脂氧合酶抑制，可能在fMLP受体或其相关转导机制水平发挥作用。
