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血小板活化因子(PAF)可诱导巨噬细胞产生氧化爆发。

Platelet activating factor (PAF) induces the oxidative burst in macrophages.

作者信息

Hartung H P, Parnham M J, Winkelmann J, Englberger W, Hadding U

出版信息

Int J Immunopharmacol. 1983;5(2):115-21. doi: 10.1016/0192-0561(83)90002-4.

Abstract

The response of guinea pig peritoneal macrophages to platelet activating factor (1-O-octadecyl-2-acetyl-sn-glycero-3-phosphoryl-choline) was examined. In Corynebacterium parvum induced macrophages, platelet activating factor, over a wide dose range (3.8 X 10(-5) to 3.8 X 10(-9)M) triggered the oxidative burst as indicated by increased luminol-dependent chemiluminescence and hydrogen peroxide release into culture supernatants. This effect of PAF was inhibited by superoxide dismutase and catalase. Resident macrophages exhibited only slight respiratory activity in response to platelet activating factor which could be increased by adding 1% gelatine to the medium. Activation of macrophages is a new biological effect exerted by platelet activating factor. In immuno-inflammatory reactions, cells capable of generating platelet activating factor may come into close contact with macrophages and by liberating this mediator cause them to release highly toxic oxygen species known to be microbicidal and cytocidal and able to produce vascular endothelial injury. Our findings lend further support to the view that platelet activating factor is a potent and rapid activator of physiological defence mechanisms.

摘要

研究了豚鼠腹腔巨噬细胞对血小板活化因子(1-O-十八烷基-2-乙酰基-sn-甘油-3-磷酸胆碱)的反应。在短小棒状杆菌诱导的巨噬细胞中,血小板活化因子在很宽的剂量范围内(3.8×10⁻⁵至3.8×10⁻⁹M)引发氧化爆发,表现为鲁米诺依赖性化学发光增加以及过氧化氢释放到培养上清液中。PAF的这种作用被超氧化物歧化酶和过氧化氢酶抑制。驻留巨噬细胞对血小板活化因子仅表现出轻微的呼吸活性,向培养基中添加1%明胶可增强这种活性。巨噬细胞的活化是血小板活化因子发挥的一种新的生物学效应。在免疫炎症反应中,能够产生血小板活化因子的细胞可能与巨噬细胞紧密接触,并通过释放这种介质使巨噬细胞释放已知具有杀菌和杀细胞作用且能够导致血管内皮损伤的高毒性氧物种。我们的研究结果进一步支持了血小板活化因子是生理防御机制的一种强效且快速的激活剂这一观点。

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