阿司匹林和非甾体抗炎药对血小板生成12-羟基二十碳四烯酸的体外作用。

In vitro effects of aspirin and non steroidal anti-inflammatory drugs on the formation of 12-hydroxyeicosatetraenoic acid by platelets.

作者信息

Tremoli E, Maderna P, Eynard A, Gregori M, Galli G

出版信息

Prostaglandins Leukot Med. 1986 Aug;23(2-3):117-22. doi: 10.1016/0262-1746(86)90173-3.

Abstract

The in vitro effects of aspirin and other non steroidal antiinflammatory drugs (NSAIDs) on 12-HETE formation were evaluated in platelet rich plasma (PRP) stimulated with collagen. Aspirin (1 X 10(-4)-1 X 10(-3) M) inhibited 12-HETE production in PRP. Inhibition of 12-HETE formation was detected also in PRP incubated with indomethacin and BW 755C. Sodium salicylate, instead, did not reduce 12-HETE synthesis. Aspirin (3 X 10(-3) M) did not modify 12-HETE synthesis in similarly challenged washed platelet (WP) preparations, inspite of its effect on the cyclooxygenase pathway. It may be concluded that aspirin and other NSAIDs, not only affect the cyclooxygenase pathway, but also inhibit 12-HETE synthesis. In addition it is shown that the 12-HETE synthesis is reduced by plasma and that this effect is enhanced in the presence of aspirin.

摘要

在富含血小板血浆（PRP）中用胶原蛋白刺激，评估阿司匹林和其他非甾体抗炎药（NSAIDs）对12 - HETE形成的体外作用。阿司匹林（1×10⁻⁴ - 1×10⁻³ M）抑制PRP中12 - HETE的产生。在用吲哚美辛和BW 755C孵育的PRP中也检测到12 - HETE形成的抑制。相反，水杨酸钠并未降低12 - HETE的合成。尽管阿司匹林（3×10⁻³ M）对环氧化酶途径有作用，但在同样受到刺激的洗涤血小板（WP）制剂中，它并未改变12 - HETE的合成。可以得出结论，阿司匹林和其他NSAIDs不仅影响环氧化酶途径，还抑制12 - HETE的合成。此外，研究表明血浆可降低12 - HETE的合成，并且在阿司匹林存在的情况下这种作用会增强。