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[磷脂酶A2、5-脂氧合酶和环氧化酶在人中性粒细胞“氧爆发”激活中的作用:培养基渗透压的调节作用]

[The role of phospholipase A2, 5-lipoxygenase, and cyclooxygenase in activation of human neutrophil "oxygen burst": the modulating effect of osmolality of the medium].

作者信息

Kuchkina N V, Orlov S N, Chuchalin A G

出版信息

Biokhimiia. 1994 Jul;59(7):1034-41.

PMID:7948413
Abstract

The roles of phospholipase A2, 5-lipoxygenase and cyclooxygenase in activation of "oxidative burst" in human neutrophils have been studied under isoosmotic (320 mOsM), hypoosmotic (200 mOsM) and hyperosmotic (420 mOsM) conditions. The oxidative burst induced by phorbol-12-myristate-13-acetate (PMA), calcium ionophore A23187 and opsonized zymosan was followed by luminol-dependent chemiluminescence (CL). There were no differences in the concentration dependences of CL inhibition at 320 mOsM and 200 mOsM in the presence of the phospholipase A2 inhibitor, p-bromphenacylbromide. Contrariwise, at 420 mOsM the sensitivity to inhibition was decreased by PMA and A23187 but increased by opsonized zymosan. A change in the medium osmolality in the presence of the 5-lipoxygenase inhibitor quercetin did not result in the modification of the concentration dependence of CL inhibition induced by any of the activators. In the presence of the cyclooxygenase inhibitor, meclofenamic acid, the "oxidative burst" induced by PMA and A23187 at 200 mOsM was manifested as a decrease of the sensitivity to inhibition, while at 420 mOsM this sensitivity was increased in comparison with that observed under isoosmotic conditions. The data obtained suggest that phospholipase A2 and cyclooxygenase play a role in the mechanism of the modulating effect of the medium osmolality on the "oxidative burst" in neutrophils, while 5-lipoxygenase is unimportant for this process.

摘要

在等渗(320毫渗量浓度)、低渗(200毫渗量浓度)和高渗(420毫渗量浓度)条件下,研究了磷脂酶A2、5-脂氧合酶和环氧化酶在人中性粒细胞“氧化爆发”激活中的作用。用佛波醇-12-肉豆蔻酸酯-13-乙酸酯(PMA)、钙离子载体A23187和调理酵母聚糖诱导氧化爆发,随后通过鲁米诺依赖的化学发光(CL)进行检测。在磷脂酶A2抑制剂对溴苯甲酰溴存在的情况下,320毫渗量浓度和200毫渗量浓度时CL抑制的浓度依赖性没有差异。相反,在420毫渗量浓度时,PMA和A23187使抑制敏感性降低,而调理酵母聚糖使其增加。在5-脂氧合酶抑制剂槲皮素存在的情况下,培养基渗透压的变化并未导致任何一种激活剂诱导的CL抑制浓度依赖性的改变。在环氧化酶抑制剂甲氯芬那酸存在的情况下,200毫渗量浓度时PMA和A23187诱导的“氧化爆发”表现为抑制敏感性降低,而在420毫渗量浓度时,与等渗条件下相比,这种敏感性增加。所获得的数据表明,磷脂酶A2和环氧化酶在培养基渗透压对中性粒细胞“氧化爆发”的调节作用机制中发挥作用,而5-脂氧合酶对该过程并不重要。

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