Possible role of arachidonic acid and its metabolites in mediator release from rat mast cells.
Possible role of arachidonic acid and its metabolites in mediator release from rat mast cells.
复制标题
花生四烯酸及其代谢物在大鼠肥大细胞介质释放中的可能作用。
DOI：
10.4049/jimmunol.122.2.431
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发表时间：
1979
影响因子：
4.4
通讯作者：
C. Parker
中科院分区：
文献类型：
--
作者：
T. Sullivan;C. Parker
研究花生四烯酸(AA)代谢在大鼠肥大细胞释放炎症介质中的作用。5，8，11，14-四元酸(Eicosa-5，8，11，14-Tetynoic acid，ETYA)可抑制抗-Ig E、刀豆蛋白A(ConA)或离子载体A-23187诱导的组胺释放，其ID_(50)值分别为65、50和17µM。浓度在60微米以下的阿司匹林或吲哚美辛不影响介质的释放。在未刺激的肥大细胞中加入游离氨基酸(0.1~100微米)不会引起非细胞毒性介质的释放。肥大细胞与1~10µM AA预孵育可抑制抗IgE或ConA诱导的后续释放(最高可达38%)。如果阿司匹林(10微米)或吲哚美辛(10微米)存在，这种释放抑制作用被阻断，这表明AA抑制是由环氧合酶产物介导的。当用抗-IgE或ConA启动分泌后再加入AA，对释放有一定的促进作用。这些研究表明，由环氧合酶以外的酶系统代谢的AA是肥大细胞分泌过程中不可或缺的一部分。然而，游离AA的可获得性似乎不是启动未受刺激细胞分泌的充分条件。由分泌信号激活的肥大细胞似乎会导致AA代谢的改变，而AA代谢又似乎参与了炎症介质的分泌。
The role of arachidonic acid (AA) metabolism in the release of inflammatory mediators from rat mast cells was studied. Eicosa-5,8,11,14-tetraynoic acid (ETYA), an acetylenic analog of AA, was found to inhibit histamine release induced by anti-IgE, concanavalin A (Con A), or the ionophore A-23187 with ID50 values of 65, 50, and 17 µM, respectively. Mediator release was not affected by aspirin or indomethacin in concentrations up to 60 µM. Addition of free AA (0.1 to 100 µM) to unstimulated mast cells did not initiate noncytotoxic mediator release. Preincubation of mast cells with 1 to 10 µM AA inhibited subsequent release induced by anti-IgE or Con A (up to 38%). This inhibition of release was blocked if aspirin (10 µM) or indomethacin (10 µM) was present, suggesting that AA inhibition was mediated by cyclo-oxygenase products. When AA was added after secretion was initiated by anti-IgE or Con A, a modest potentiation of release was noted. These studies suggest that AA metabolism by enzyme systems other than cyclo-oxygenase is an integral part of the mast cell secretory process. Availability of free AA, however, does not appear to be a sufficient condition to initiate secretion by otherwise unstimulated cells. Activation of mast cells by secretory signals appears to lead to altered AA metabolism which in turn appears to be involved in the secretion of inflammatory mediators.