Platelet-activating factor-induced aggregation of human platelets specifically inhibited by triazolobenzodiazepines.
Platelet-activating factor-induced aggregation of human platelets specifically inhibited by triazolobenzodiazepines.
复制标题
血小板激活因子诱导的人血小板聚集被三唑并苯二氮卓类药物特异性抑制。
DOI：
10.1126/science.6150550
复制
发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Lenox,RH
中科院分区：
文献类型：
--
作者：
Kornecki,E;Ehrlich,YH;Lenox,RH
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多种生物过程的有效激活剂。PAF的作用机制在很大程度上是未知的，部分原因是缺乏PAF引发的反应的特定抑制剂。在洗涤的人血小板中，精神药物阿普唑仑和三唑仑能有效地抑制PAF诱导的形状、聚集和分泌的变化。由于三唑苯二氮类药物不抑制人血小板对二磷酸腺苷、凝血酶、肾上腺素、胶原、花生四烯酸和钙离子载体A23187的反应，因此这种作用是PAF激活所特有的。这些精神药物将有助于研究PAF或PAF样磷脂在神经元功能中发挥作用的可能性，并有助于阐明PAF在各种细胞中特异激活的生化机制。
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.