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甲硫氨酸脑啡肽和亮氨酸脑啡肽对人多形核白细胞超氧阴离子释放的调节作用。

Modulation of superoxide anion release from human polymorphonuclear cells by Met- and Leu-enkephalin.

作者信息

Marotti T, Sverko V, Hrsak I

机构信息

Department of Experimental Biology and Medicine, Rudjer Bosković Institute, Zagreb, Yugoslavia.

出版信息

Brain Behav Immun. 1990 Mar;4(1):13-22. doi: 10.1016/0889-1591(90)90002-8.

DOI:10.1016/0889-1591(90)90002-8
PMID:2159354
Abstract

The present work describes the ability of Met- and Leu-enkephalin to modulate the superoxide anion (O2-) release from unstimulated human polymorphonuclear cells (PMN) and from PMN stimulated with phorbol myristate acetate (PMA). The direction (stimulation or suppression) and the magnitude of change were dependent upon the baseline reactivity of the donor's PMN. Both opioid peptides stimulated O2- release by PMN from donors with low baseline reactivity in a concentration-dependent manner. PMNs collected from donors with medium baseline reactivity incubated with Leu-enkephalin regardless of concentration released less O2- than control, nontreated PMNs. Met-enkephalin stimulated O2- release but only at 2 X 10(-15) M concentration. Superoxide anion release from PMNs of individuals with high baseline reactivity was concentration dependent and suppressed by Met- and Leu-enkephalin. Leu-enkephalin induced baseline reactivity was dependent upon progressive increase in the magnitude of change on O2- release (i.e., the higher the baseline the higher the magnitude of change in O2- generation). Met-enkephalin data show this also, but to a lesser extent. In cells stimulated with PMA, Met-enkephalin caused additional O2- release, while Leu-enkephalin was ineffective in triggering already stimulated cells. The modulating effect of both opioid peptides on superoxide anion release by human PMN is a short phenomenon that lasts up to 10 min after the addition of the peptide.

摘要

本研究描述了甲硫氨酸脑啡肽和亮氨酸脑啡肽对未受刺激的人多形核白细胞(PMN)以及用佛波酯十四烷酸酯(PMA)刺激的PMN释放超氧阴离子(O2-)的调节能力。变化的方向(刺激或抑制)和幅度取决于供体PMN的基线反应性。两种阿片肽均以浓度依赖性方式刺激基线反应性较低的供体的PMN释放O2-。与亮氨酸脑啡肽孵育的、来自基线反应性中等的供体的PMN,无论浓度如何,其释放的O2-均少于未处理的对照PMN。甲硫氨酸脑啡肽仅在2×10^(-15) M浓度时刺激O2-释放。基线反应性高的个体的PMN释放超氧阴离子呈浓度依赖性,并受到甲硫氨酸脑啡肽和亮氨酸脑啡肽的抑制。亮氨酸脑啡肽诱导的基线反应性取决于O2-释放变化幅度的逐渐增加(即基线越高,O2-生成的变化幅度越高)。甲硫氨酸脑啡肽的数据也显示了这一点,但程度较小。在用PMA刺激的细胞中,甲硫氨酸脑啡肽导致额外的O2-释放,而亮氨酸脑啡肽对已被刺激的细胞无触发作用。两种阿片肽对人PMN释放超氧阴离子的调节作用是一种短暂现象,在添加肽后可持续长达10分钟。

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