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[酮替芬对兔血小板聚集及大鼠中性粒细胞血小板活化因子生成的影响]

[Effects of ketotifen on rabbit platelet aggregation and platelet activating factor formation from rat neutrophils].

作者信息

Wang X D, Bian R L

机构信息

Department of Pharmacology, Zhejiang Medical University, Hangzhou, China.

出版信息

Zhongguo Yao Li Xue Bao. 1990 Nov;11(6):524-7.

PMID:2130617
Abstract

The effects of ketotifen (Ket) on rabbit platelet aggregation induced by platelet activating factor (PAF), ADP and arachidonic acid (AA) and PAF formation from A-23187-stimulated rat neutrophils in vitro were studied. PAF (15-100 pmol/L) induced rabbit platelet aggregations, with an EC50 of 33 pmol/L. Ket shifted the PAF dose-dependent platelet aggregation curve to the right in a parallel fashion with no depression of the maximal response and reversed the secondary aggregation phase, suggesting that Ket had competitive antagonistic activity against PAF-induced platelet aggregation. It also showed inhibitory effects on platelet aggregations induced by ADP 10 mumol/L and AA 50 mumol/L, the IC50 were 94.5 and 143.5 mumol/L respectively. However, it failed to influence PAF formation from rat neutrophils stimulated by A-23187 2.5 mumol/L in vitro. The inhibitory effects of Ket on platelet activation, particularly PAF-induced platelet aggregation, may contribute to its anti-asthmatic properties.

摘要

研究了酮替芬(Ket)对血小板活化因子(PAF)、二磷酸腺苷(ADP)和花生四烯酸(AA)诱导的兔血小板聚集以及体外A-23187刺激的大鼠中性粒细胞PAF形成的影响。PAF(15 - 100 pmol/L)诱导兔血小板聚集,半数有效浓度(EC50)为33 pmol/L。Ket使PAF剂量依赖性血小板聚集曲线平行右移,最大反应无降低,并逆转了继发性聚集阶段,表明Ket对PAF诱导的血小板聚集具有竞争性拮抗活性。它对10 μmol/L ADP和50 μmol/L AA诱导的血小板聚集也有抑制作用,半数抑制浓度(IC50)分别为94.5和143.5 μmol/L。然而,它未能影响体外2.5 μmol/L A-23187刺激的大鼠中性粒细胞PAF的形成。Ket对血小板活化的抑制作用,尤其是对PAF诱导的血小板聚集的抑制作用,可能有助于其抗哮喘特性。

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