[nadph氧化酶与巨噬细胞产生活性氧]。

Ceskoslovenska fysiologie Pub Date : 2012-01-01
M Zaloudiková
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引用次数: 0

摘要

巨噬细胞不仅在抵抗感染中发挥重要作用,而且参与许多不同的病理过程。它们在低氧性肺动脉高压(HPH)的发展中起着重要作用。巨噬细胞产生活性氧(ROS)导致肺组织损伤,似乎在这一过程中起关键作用。本文主要研究了肺泡巨噬细胞中nadph氧化酶衍生的ROS的产生及其修饰方法。nadph氧化酶通过两种不同的途径被许多刺激物激活。触发器的作用,除了其他,可以发挥整合素,分子调解细胞的粘附。为了测试粘附的作用,我们比较了肺泡和腹膜巨噬细胞的ROS生成(通过发光依赖性化学发光(LDCL)以释放过氧化氢的量来测量)。粘附本身仅在肺泡巨噬细胞中显著触发H2O2的产生。因此,我们认为粘附仅在肺泡巨噬细胞中被识别为病理信号,并且它可以改变巨噬细胞对进一步刺激的反应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[NADPH-oxidase and the reactive oxygen species production by macrophages].

Macrophages play an essential role not only in the defense against the infection, but are involved in many various pathological processes. They take an important part, e.g., in the development of hypoxic pulmonary hypertension (HPH). The production of reactive oxygen species (ROS) by macrophages causes the pulmonary tissue damage, which seems to play a key role in this process. This paper is focused on the NADPH-oxidase derived ROS production in alveolar macrophages and ways of its modification. NADPH-oxidase is activated via two different pathways by many stimulators. The role of the trigger can play, besides others, integrins, molecules mediating the adherence of cells. To test a role of adherence, we compared ROS production (measured as the amount of released hydrogen peroxide by the luminoldependent chemiluminescence (LDCL)) in alveolar and peritoneal macrophages. The adherence itself triggered significantly the H2O2 production only in the alveolar macrophages. Thus we suppose that the adherence is recognised as the pathological signal only in the alveolar macrophages and it can modify macrophages response to further stimuli.

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