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乙醇会影响人多形核粒细胞中白三烯的生成以及白三烯诱导的功能反应。

Ethanol affects leukotriene generation and leukotriene-induced functional responses in human polymorphonuclear granulocytes.

作者信息

Nilsson E, Edenius C, Lindgren J A

机构信息

Department of Medicine, Karolinska Institute at Stockholm Söder Hospital, Sweden.

出版信息

Scand J Clin Lab Invest. 1995 Nov;55(7):589-96. doi: 10.3109/00365519509110258.

DOI:10.3109/00365519509110258
PMID:8633183
Abstract

Since ethanol has been shown to inhibit the inflammatory response, we evaluated whether ethanol affected generation of leukotrienes in polymorphonuclear granulocytes (PMN) in vitro. Using the calcium ionophore A23187 as stimulus, the leukotriene B4 (LTB4) and leukotriene C4 (LTC4) generation were dose-dependently impaired by ethanol. No significant difference in the levels of the omega-oxidized metabolites was observed. However, the total LTB4 production (LTB4 plus omega-oxidized metabolites) was significantly decreased in the samples treated with ethanol. Furthermore, ethanol also modulated LTB4-induced functional responses. PMN aggregation, oxidative metabolism and elastase release were all inhibited in the presence of 1% ethanol (to 74 +/- 15%, 50 +/- 4% and 57 +/- 3% of controls, respectively). However, ethanol had no effect on intracellular calcium mobilization or on the change of the PMN membrane potential induced by either LTB4 or A23187. Thus, a possible mechanism for the reduced functional PMN responses in the presence of ethanol might be impaired generation of leukotrienes, but it is conceivable that ethanol impairs also other steps of the stimulus response coupling since the LTB4-induced functional responses were inhibited.

摘要

由于乙醇已被证明可抑制炎症反应,我们评估了乙醇在体外是否会影响多形核粒细胞(PMN)中白三烯的生成。以钙离子载体A23187作为刺激物,乙醇可剂量依赖性地损害白三烯B4(LTB4)和白三烯C4(LTC4)的生成。未观察到ω-氧化代谢产物水平的显著差异。然而,在用乙醇处理的样本中,LTB4的总生成量(LTB4加上ω-氧化代谢产物)显著降低。此外,乙醇还调节了LTB4诱导的功能反应。在1%乙醇存在的情况下,PMN聚集、氧化代谢和弹性蛋白酶释放均受到抑制(分别降至对照组的74±15%、50±4%和57±3%)。然而,乙醇对细胞内钙动员或LTB4或A23187诱导的PMN膜电位变化没有影响。因此,乙醇存在时PMN功能反应降低的一种可能机制可能是白三烯生成受损,但可以想象,乙醇也会损害刺激反应偶联的其他步骤,因为LTB4诱导的功能反应受到了抑制。

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