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维生素E对乙酰水杨酸在人体血液中抗血小板作用的影响。

Influence of vitamin E on the antiplatelet effect of acetylsalicylic acid in human blood.

作者信息

González-Correa J A, Arrebola M M, Guerrero A, Muñoz-Marín J, Ruiz-Villafranca D, Sánchez de La Cuesta F, De La Cruz J P

机构信息

Department of Pharmacology and Therapeutics, School of Medecine, University of Málaga, Campus de Teatinos s/n, Málaga, Spain.

出版信息

Platelets. 2005 May-Jun;16(3-4):171-9. doi: 10.1080/09537100400016797.

Abstract

We analysed the in vitro interaction between acetylsalicylic acid and vitamin E on the principal antiplatelet sites of action of acetylsalicylic acid, i.e., platelet aggregation, prostanoid production in platelets and leukocytes, and nitric oxide synthesis. Aggregation was measured in whole blood and in platelet-rich plasma (PRP) with ADP, collagen or arachidonic acid as platelet inducers, and we measured the production of thromboxane B2, prostacyclin and nitric oxide. Vitamin E potentiated the antiplatelet effect of acetylsalicylic acid in both whole blood and PRP. In PRP induced with collagen the IC50 for acetylsalicylic acid alone was 339+/-11.26, and that of acetylsalicylic acid+vitamin E was 0.89+/-0.09 (P<0.05). Vitamin E did not enhance inhibition of platelet thromboxane production by acetylsalicylic acid. Vitamin E spared or even increased prostacyclin levels, and acetylsalicylic acid+vitamin E diminished the inhibition of prostacyclin synthesis by acetylsalicylic acid (IC50 acetylsalicylic acid alone=1.81+/-0.15 microM; IC50 acetylsalicylic acid+vitamin E= 12.92+/-1.10 microM, P<0.05). Vitamin E increased the effect of acetylsalicylic acid on neutrophil nitric oxide production 42-fold (P<0.05). We conclude that vitamin E potentiates the antiplatelet effect of acetylsalicylic acid in vitro, and thus merits further research in ex vivo studies.

摘要

我们分析了乙酰水杨酸与维生素E在乙酰水杨酸主要抗血小板作用位点上的体外相互作用,即血小板聚集、血小板和白细胞中前列腺素的生成以及一氧化氮的合成。使用ADP、胶原或花生四烯酸作为血小板诱导剂,在全血和富血小板血浆(PRP)中测量聚集情况,并测定血栓素B2、前列环素和一氧化氮的生成。维生素E增强了乙酰水杨酸在全血和PRP中的抗血小板作用。在由胶原诱导的PRP中,单独乙酰水杨酸的IC50为339±11.26,而乙酰水杨酸+维生素E的IC50为0.89±0.09(P<0.05)。维生素E并未增强乙酰水杨酸对血小板血栓素生成的抑制作用。维生素E使前列环素水平得以保留甚至升高,并且乙酰水杨酸+维生素E减弱了乙酰水杨酸对前列环素合成的抑制作用(单独乙酰水杨酸的IC50 = 1.81±0.15微摩尔;乙酰水杨酸+维生素E的IC50 = 12.92±1.10微摩尔,P<0.05)。维生素E使乙酰水杨酸对中性粒细胞一氧化氮生成的作用增强了42倍(P<0.05)。我们得出结论,维生素E在体外增强了乙酰水杨酸的抗血小板作用,因此值得在体外研究中进一步开展研究。

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