奈多罗米钠对血小板活化因子诱导人中性粒细胞产生超氧化物的差异抑制作用。
Differential inhibition by nedocromil sodium of superoxide generation elicited by platelet activating factor in human neutrophils.
作者信息
Rubin R P, Thompson R H, Naps M S
机构信息
Department of Pharmacology and Toxicology, Medical College of Virginia, Richmond 23298.
出版信息
Agents Actions. 1990 Nov;31(3-4):237-42. doi: 10.1007/BF01997614.
Nedocromil sodium (10(-10) - 10(-9) M) produced a dose-related inhibition of superoxide anion generation induced by platelet activating factor (PAF) in human polymorphonuclear leukocytes (PMNs). At a higher concentration (3 x 10(-7) M), nedocromil sodium significantly inhibited superoxide generation elicited by N-formyl-methionyl-leucylphenylalanine, but was unable to block the response to phorbol dibutyrate. Nedocromil sodium (10(-11) - 10(-5) M) enhanced PAF-stimulated lysozyme release in a non-concentration-dependent manner, and was completely ineffective in depressing PAF-induced release of [3H]arachidonic acid and the rise in cytosolic Ca2+. The preferential inhibitory effects of nedocromil sodium on PAF-induced activation of superoxide generation may provide insight into the therapeutic action of this drug as an anti-asthmatic agent.
奈多罗米钠（10⁻¹⁰ - 10⁻⁹ M）对血小板活化因子（PAF）诱导的人多形核白细胞（PMN）中超氧化物阴离子的生成产生剂量相关的抑制作用。在较高浓度（3×10⁻⁷ M）时，奈多罗米钠显著抑制N-甲酰甲硫氨酰亮氨酰苯丙氨酸引发的超氧化物生成，但无法阻断对佛波酯的反应。奈多罗米钠（10⁻¹¹ - 10⁻⁵ M）以非浓度依赖性方式增强PAF刺激的溶菌酶释放，并且在抑制PAF诱导的[³H]花生四烯酸释放和胞质Ca²⁺升高方面完全无效。奈多罗米钠对PAF诱导的超氧化物生成激活的优先抑制作用可能有助于深入了解该药物作为抗哮喘药物的治疗作用。
Zotero 插件