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三唑并苯二氮䓬类药物特异性抑制血小板活化因子诱导的人血小板聚集。

Platelet-activating factor-induced aggregation of human platelets specifically inhibited by triazolobenzodiazepines.

作者信息

Kornecki E, Ehrlich Y H, Lenox R H

出版信息

Science. 1984 Dec 21;226(4681):1454-6. doi: 10.1126/science.6150550.

Abstract

Platelet-activating factor (PAF), a naturally occurring phospholipid, is a potent activator of various biological processes, including platelet aggregation. The mechanisms by which PAF acts are largely unknown, partly because of the lack of specific inhibitors for PAF-elicited responses. It was found that in washed human platelets the psychotropic triazolobenzodiazepine drugs alprazolam and triazolam potently inhibited PAF-induced changes in shape, aggregation, and secretion. The effects were specific for PAF activation, since the responses of human platelets to adenosine diphosphate, thrombin, epinephrine, collagen, arachidonate, and the calcium ionophore A23187 were not inhibited by the triazolobenzodiazepines. These psychotropic drugs should be useful in investigating the possibility that PAF or PAF-like phospholipids play a role in neuronal function and in elucidating biochemical mechanisms activated specifically by PAF in a variety of cells.

摘要

血小板活化因子(PAF)是一种天然存在的磷脂,是包括血小板聚集在内的各种生物过程的强效激活剂。PAF发挥作用的机制在很大程度上尚不清楚,部分原因是缺乏针对PAF引发反应的特异性抑制剂。研究发现,在洗涤过的人血小板中,精神类三唑并苯二氮䓬药物阿普唑仑和三唑仑能有效抑制PAF诱导的形态、聚集和分泌变化。这些作用对PAF激活具有特异性,因为人血小板对二磷酸腺苷、凝血酶、肾上腺素、胶原蛋白、花生四烯酸和钙离子载体A23187的反应不受三唑并苯二氮䓬类药物的抑制。这些精神类药物在研究PAF或PAF样磷脂在神经元功能中发挥作用的可能性以及阐明PAF在各种细胞中特异性激活的生化机制方面应该是有用的。

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