Bates E J, Harvey D P, Ferrante A
Department of Immunology, Adelaide Children's Hospital, Australia.
Int Arch Allergy Immunol. 1992;97(1):50-6. doi: 10.1159/000236095.
The effect of three platelet-activating factor (PAF) antagonists, WEB 2086, CV 6209 and CV 3988, on neutrophil respiratory burst activity and degranulation in response to PAF was investigated. Both WEB 2086 and CV 6209 significantly inhibited the respiratory burst and degranulation in response to 400 nM PAF in a dose-dependent manner (10(-8)-10(-5) M). Higher concentrations of CV 3988 were required to inhibit these functions (10(-5) M and above). The three antagonists inhibited both the release of beta-glucuronidase (from azurophilic granules) and vitamin B12 binding protein (from specific granules) in response to PAF. Only a small nonsignificant inhibition of neutrophil function occurred in the absence of PAF. There was no loss of viability after incubation with the three antagonists at the concentrations tested. These antagonists will be useful tools to study the involvement of PAF in neutrophil-mediated tissue damage and inflammation.
研究了三种血小板活化因子（PAF）拮抗剂WEB 2086、CV 6209和CV 3988对中性粒细胞呼吸爆发活性以及对PAF反应性脱颗粒的影响。WEB 2086和CV 6209均以剂量依赖性方式（10⁻⁸ - 10⁻⁵ M）显著抑制对400 nM PAF的呼吸爆发和脱颗粒。抑制这些功能需要更高浓度的CV 3988（10⁻⁵ M及以上）。这三种拮抗剂均抑制对PAF反应性的β-葡萄糖醛酸酶（来自嗜天青颗粒）和维生素B₁₂结合蛋白（来自特异性颗粒）的释放。在无PAF的情况下，仅出现对中性粒细胞功能的轻微非显著性抑制。在所测试的浓度下，与这三种拮抗剂孵育后细胞活力没有丧失。这些拮抗剂将成为研究PAF在中性粒细胞介导的组织损伤和炎症中所起作用的有用工具。
