Umeki S, Soejima R
Department of Medicine, Kawasaki Medical School.
Kansenshogaku Zasshi. 1990 Sep;64(9):1184-91. doi: 10.11150/kansenshogakuzasshi1970.64.1184.
The effects of anti-inflammatory drugs (acetylsalicylic acid, ASA; salicylic acid, SA; indomethacin, IM; hydrocortisone, HC) on the respiratory burst oxidase (NADPH oxidase) from human neutrophils in both whole cell and fully soluble (cell-free) systems were investigated. These drugs were found to inhibit the superoxide generation by human neutrophils exposed to phorbol myristate acetate in a whole cell system and the activation of superoxide-generating NADPH oxidase by sodium dodecyl sulfate in cell-free systems. Concentrations of these drugs required for 50% inhibition of the oxidase (ID50) were; ASA (more than 3.0 mM in the whole cell system and 1.35 mM in the cell-free system), SA (more than 3.0 mM in the whole cell system and 1.30 mM in the cell-free system), IM (180 microM in both systems) and HC (50 microM in the whole cell system and 40 microM in the cell-free system). In addition, these drugs time-dependently inhibited the activation of NADPH oxidase in cell-free systems. In the cell-free system, all of the drugs did not change the Km values for NADPH of the oxidase. These results suggest that these anti-inflammatory drugs, especially HC and IM, inhibit the reconstitution (activation) of neutrophil NADPH oxidase enzyme in the cell-free (whole cell) system.
研究了抗炎药物（乙酰水杨酸，ASA；水杨酸，SA；吲哚美辛，IM；氢化可的松，HC）在全细胞和完全可溶（无细胞）系统中对人中性粒细胞呼吸爆发氧化酶（NADPH氧化酶）的影响。发现在全细胞系统中，这些药物可抑制暴露于佛波酯肉豆蔻酸酯的人中性粒细胞产生超氧化物，在无细胞系统中可抑制十二烷基硫酸钠对产生超氧化物的NADPH氧化酶的激活。这些药物对氧化酶50%抑制所需的浓度（ID50）分别为：ASA（全细胞系统中大于3.0 mM，无细胞系统中为1.35 mM），SA（全细胞系统中大于3.0 mM，无细胞系统中为1.30 mM），IM（两个系统中均为180 microM）和HC（全细胞系统中为50 microM，无细胞系统中为40 microM）。此外，这些药物在无细胞系统中对NADPH氧化酶的激活具有时间依赖性抑制作用。在无细胞系统中，所有药物均未改变氧化酶对NADPH的Km值。这些结果表明，这些抗炎药物，尤其是HC和IM，在无细胞（全细胞）系统中抑制中性粒细胞NADPH氧化酶的重组（激活）。
