前列腺素E1对人中性粒细胞功能的抑制作用。

Inhibitory effect of prostaglandin E1 on human neutrophil function.

作者信息

Mikawa K, Akamatsu H, Maekawa N, Nishina K, Obara H, Niwa Y

机构信息

Department of Anaesthesiology, Kobe University School of Medicine, Japan.

出版信息

Prostaglandins Leukot Essent Fatty Acids. 1994 Oct;51(4):287-91. doi: 10.1016/0952-3278(94)90193-7.

DOI:10.1016/0952-3278(94)90193-7

PMID:7846097

Abstract

Neutrophils accumulated in the lung are thought to play a pivotal role in the pathogenesis of host auto-injury such as adult respiratory distress syndrome (ARDS). We investigated the effect of prostaglandin E1 (PGE1) on several aspects of human neutrophil function. PGE1 significantly decreased reactive oxygen species (ROS), (O2-, H2O2, OH.) generation by neutrophils as well as neutrophil phagocytosis and chemotaxis. In contrast, the drug did not affect the levels of ROS generated by a cell-free ROS generating system. In addition, intracellular calcium concentrations ([Ca2+]i) in neutrophils stimulated by f-Met-Leu-Phe were decreased in the presence of PGE1. These data suggest that the reduction in ROS production and neutrophil phagocytosis and chemotaxis by PGE1 may contribute to the effectiveness of the drug in host auto-injury including ARDS. The suppression of the increase in [Ca2+]i may at least be responsible for inhibition of these neutrophil functions by PGE1.

摘要

积聚在肺部的中性粒细胞被认为在诸如成人呼吸窘迫综合征（ARDS）等宿主自身损伤的发病机制中起关键作用。我们研究了前列腺素E1（PGE1）对人中性粒细胞功能多个方面的影响。PGE1显著降低了中性粒细胞产生的活性氧（ROS）（超氧阴离子、过氧化氢、羟自由基），以及中性粒细胞的吞噬作用和趋化性。相比之下，该药物不影响无细胞ROS生成系统产生的ROS水平。此外，在PGE1存在的情况下，由f-Met-Leu-Phe刺激的中性粒细胞内钙浓度（[Ca2+]i）降低。这些数据表明，PGE1降低ROS生成、中性粒细胞吞噬作用和趋化性可能有助于该药物在包括ARDS在内的宿主自身损伤中发挥作用。[Ca2+]i升高的抑制至少可能是PGE1抑制这些中性粒细胞功能的原因。