Moqbel R, Cromwell O, Kay A B
Department of Allergy and Clinical Immunology, National Heart and Lung Institute, London, United Kingdom.
Drugs. 1989;37 Suppl 1:19-22; discussion 69-77. doi: 10.2165/00003495-198900371-00005.
Nedocromil sodium inhibited the increase in eosinophil activation (measured by IgG- and complement-dependent cytotoxicity assays) induced by platelet activating factor (PAF). Inhibition of the upregulation in eosinophil effector function by nedocromil sodium was dose-dependent (optimal at 10(-7) mol/L) and paralleled that produced by a specific PAF antagonist, BN 52021. In addition, preliminary data suggest that nedocromil sodium can inhibit the increase in IgG-dependent release of LTC4 from human eosinophils after stimulation with the synthetic tripeptide, formyl-methionyl-leucyl-phenylalanine (fMLP). These data support our previous hypothesis that part of the mode of action of nedocromil sodium may be due to its ability to directly block the chemotactic factor-induced enhancement of inflammatory cell activity.
奈多罗米钠可抑制血小板活化因子（PAF）诱导的嗜酸性粒细胞活化增加（通过IgG和补体依赖性细胞毒性测定法测量）。奈多罗米钠对嗜酸性粒细胞效应功能上调的抑制作用呈剂量依赖性（在10⁻⁷mol/L时最佳），且与特异性PAF拮抗剂BN 52021产生的抑制作用相似。此外，初步数据表明，奈多罗米钠可抑制合成三肽甲酰甲硫氨酰亮氨酰苯丙氨酸（fMLP）刺激后人嗜酸性粒细胞中IgG依赖性白三烯C4释放的增加。这些数据支持了我们之前的假设，即奈多罗米钠的部分作用方式可能是由于其直接阻断趋化因子诱导的炎症细胞活性增强的能力。
