作者: JIH-HWA GUH , FENG-NIEN KO , TING-TING JONG , CHE-MING TENG
DOI: 10.1111/J.2042-7158.1995.TB05804.X
关键词: Chemistry 、 Biochemistry 、 Platelet aggregation inhibitor 、 Adenosine 、 Arachidonic acid 、 Pharmacology 、 Thromboxane B2 、 Thrombin 、 Platelet 、 Gingerol 、 Thromboxane
摘要: The purpose of this investigation was to determine the antiplatelet mechanism gingerol. Gingerol concentration-dependently (0.5-20 microM) inhibited aggregation and release reaction rabbit washed platelets induced by arachidonic acid collagen, but not those platelet-activating factor (PAF), U46619 (9,11-dideoxy-9 alpha,11 alpha-methano-epoxy-PGF2 alpha) thrombin. also (0.5-10 thromboxane B2 prostaglandin D2 formation caused acid, completely abolished phosphoinositide breakdown had no effect on that PAF or thrombin even at concentrations as high 300 microM. In human platelet-rich plasma, gingerol indomethacin prevented secondary blocked ATP from adenosine 5'-diphosphate (ADP, 5 adrenaline (5 influence primary aggregation. maximal obtained when were incubated with for 30 min inhibition reversible. It is concluded action mainly due formation.