Guh J H, Ko F N, Jong T T, Teng C M
Pharmacological Institute, College of Medicine, National Taiwan University, Taipei, Taiwan.
J Pharm Pharmacol. 1995 Apr;47(4):329-32. doi: 10.1111/j.2042-7158.1995.tb05804.x.
The purpose of this investigation was to determine the antiplatelet mechanism of gingerol. Gingerol concentration-dependently (0.5-20 microM) inhibited the aggregation and release reaction of rabbit washed platelets induced by arachidonic acid and collagen, but not those induced by platelet-activating factor (PAF), U46619 (9,11-dideoxy-9 alpha,11 alpha-methano-epoxy-PGF2 alpha) and thrombin. Gingerol also concentration-dependently (0.5-10 microM) inhibited thromboxane B2 and prostaglandin D2 formation caused by arachidonic acid, and completely abolished phosphoinositide breakdown induced by arachidonic acid but had no effect on that of collagen, PAF or thrombin even at concentrations as high as 300 microM. In human platelet-rich plasma, gingerol and indomethacin prevented the secondary aggregation and blocked ATP release from platelets induced by adenosine 5'-diphosphate (ADP, 5 microM) and adrenaline (5 microM) but had no influence on the primary aggregation. The maximal antiplatelet effect was obtained when platelets were incubated with gingerol for 30 min and this inhibition was reversible. It is concluded that the antiplatelet action of gingerol is mainly due to the inhibition of thromboxane formation.
本研究的目的是确定姜辣素的抗血小板机制。姜辣素浓度依赖性地（0.5 - 20微摩尔）抑制花生四烯酸和胶原诱导的兔洗涤血小板的聚集和释放反应，但不抑制血小板活化因子（PAF）、U46619（9,11 - 二脱氧 - 9α,11α - 甲撑环氧 - PGF2α）和凝血酶诱导的反应。姜辣素还浓度依赖性地（0.5 - 10微摩尔）抑制花生四烯酸引起的血栓素B2和前列腺素D2的形成，并完全消除花生四烯酸诱导的磷脂酰肌醇分解，但即使在高达300微摩尔的浓度下，对胶原、PAF或凝血酶诱导的磷脂酰肌醇分解也没有影响。在富含人血小板的血浆中，姜辣素和吲哚美辛可防止由5'-二磷酸腺苷（ADP，5微摩尔）和肾上腺素（5微摩尔）诱导的血小板继发性聚集并阻止ATP释放，但对原发性聚集没有影响。当血小板与姜辣素孵育30分钟时可获得最大抗血小板作用，且这种抑制作用是可逆的。结论是，姜辣素的抗血小板作用主要是由于抑制血栓素的形成。
