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首页> 外文期刊>Brazilian Journal of Medical and Biological Research >Effect of therapeutic plasma concentrations of non-steroidal anti-inflammatory drugs on the production of reactive oxygen species by activated rat neutrophils
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Effect of therapeutic plasma concentrations of non-steroidal anti-inflammatory drugs on the production of reactive oxygen species by activated rat neutrophils

机译：血浆非甾体类抗炎药的治疗浓度对活化的大鼠中性粒细胞产生活性氧的影响

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The release of reactive oxygen specie (ROS) by activated neutrophil is involved in both the antimicrobial and deleterious effects in chronic inflammation. The objective of the present investigation was to determine the effect of therapeutic plasma concentrations of non-steroidal anti-inflammatory drugs (NSAIDs) on the production of ROS by stimulated rat neutrophils. Diclofenac (3.6 μM), indomethacin (12 μM), naproxen (160 μM), piroxicam (13 μM), and tenoxicam (30 μM) were incubated at 37oC in PBS (10 mM), pH 7.4, for 30 min with rat neutrophils (1 x 10(6) cells/ml) stimulated by phorbol-12-myristate-13-acetate (100 nM). The ROS production was measured by luminol and lucigenin-dependent chemiluminescence. Except for naproxen, NSAIDs reduced ROS production: 58 ± 2% diclofenac, 90 ± 2% indomethacin, 33 ± 3% piroxicam, and 45 ± 6% tenoxicam (N = 6). For the lucigenin assay, naproxen, piroxicam and tenoxicam were ineffective. For indomethacin the inhibition was 52 ± 5% and diclofenac showed amplification in the light emission of 181 ± 60% (N = 6). Using the myeloperoxidase (MPO)/H2O2/luminol system, the effects of NSAIDs on MPO activity were also screened. We found that NSAIDs inhibited both the peroxidation and chlorinating activity of MPO as follows: diclofenac (36 ± 10, 45 ± 3%), indomethacin (97 ± 2, 100 ± 1%), naproxen (56 ± 8, 76 ± 3%), piroxicam (77 ± 5, 99 ± 1%), and tenoxicam (90 ± 2, 100 ± 1%), respectively (N = 3). These results show that therapeutic levels of NSAIDs are able to suppress the oxygen-dependent antimicrobial or oxidative functions of neutrophils by inhibiting the generation of hypochlorous acid.
机译：活化的中性粒细胞释放活性氧（ROS）参与慢性炎症的抗微生物和有害作用。本研究的目的是确定非甾体抗炎药（NSAIDs）的治疗性血浆浓度对受刺激的大鼠中性粒细胞产生ROS的影响。将双氯芬酸（3.6μM），消炎痛（12μM），萘普生（160μM），吡罗昔康（13μM）和替诺昔康（30μM）在37°C的PBS（10 mM），pH 7.4中与大鼠中性粒细胞孵育30分钟。 （1 x 10（6）个细胞/ ml）被佛波醇12-肉豆蔻酸酯13-乙酸酯（100 nM）刺激。 ROS的产生是通过鲁米诺和依赖于光泽精的化学发光来测量的。除萘普生外，NSAIDs降低ROS产生：58±2％双氯芬酸，90±2％消炎痛，33±3％吡罗昔康和45±6％替诺昔康（N = 6）。对于光泽精测定，萘普生，吡罗昔康和替诺昔康无效。对于消炎痛，抑制率为52±5％，双氯芬酸在181±60％的发光中显示出放大（N = 6）。使用髓过氧化物酶（MPO）/ H2O2 /鲁米诺系统，还筛选了NSAIDs对MPO活性的影响。我们发现NSAIDs可同时抑制MPO的过氧化和氯化活性：双氯芬酸（36±10，45±3％），消炎痛（97±2、100±1％），萘普生（56±8、76±3％） ），吡罗昔康（77±5，99±1％）和替诺昔康（90±2，100±1％）（N = 3）。这些结果表明，治疗水平的非甾体抗炎药能够通过抑制次氯酸的产生来抑制中性粒细胞的氧依赖性抗菌或氧化功能。

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