数字农科院2.0

Aspirin Eugenol Ester Inhibits Agonist-Induced P.latelet Aggregation In Vitro B y Regulating Pi3K/Akt, Mapk And Sirt 1/Cd40L Pathways

文献类型： 外文期刊

作者： Li, Jian-Yong;Dong-Shuai Shen

作者机构：

关键词： AEE; Platelets; Akt; Sirt 1; MAPK

期刊名称： EUROPEAN JOURNAL OF PHARMACOLOGY

ISSN： 0014-2999

年卷期： 2019 年 852 卷

页码：

摘要： Aspirin eugenol ester (AEE) was a promising drug candidate for treating inflammation, pain and fever and preventing cardiovascular diseases with fewer side effects than its precursors. Previous researches indicated that AEE could markedly inhibit agonist-induced platelet aggregation in vitro and ex vivo, however, the anti-platelet aggregation mechanisms of AEE remain to be defined. Here, AEE in vitro effects on agonist-induced granule-secretion, intercellular Ca2+ mobilization and thromboxane A(2) (TXA(2)) generation were examined. Vasodilator-stimulated phosphoprotein (VASP), mitogen-activated protein kinase (MAPK), Akt, Sirt 1 and CD40L expressions were also studied. In agonist-activated platelets in vitro, AEE markedly attenuated granule secretion markers (P-selectin expression and ATP release), intercellular Ca2+ mobilization and thromboxane B-2 (TXB2) formation. AEE also attenuated CD40L activation, suppressed extracellular-signal-regulated protein kinase 2 (ERK2), c-Jun N-terminal kinase 1 (JNK1) and Akt phosphorylation, and recovered Sirt1 expression, but the activation of p38, VASP(ser157) and VASP(ser239), and the levels of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) were not affected by AEE. Overall, this study demonstrates that AEE inhibits agonist-induced platelet aggregation in vitro by regulating PI3K/Akt, MAPK and Sirt 1/CD40L pathways.

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