Wu C C, Ko F N, Wu T S, Teng C M
Pharmacological Institute, College of Medicine, National Taiwan University, Taipei.
Biochim Biophys Acta. 1994 Sep 28;1201(1):1-6. doi: 10.1016/0304-4165(94)90142-2.
Clausine-D inhibited concentration-dependently the aggregation and release reaction of washed rabbit platelets induced by arachidonic acid and collagen, without affecting those induced by U46619, PAF and thrombin. The IC50 values of clausine-D on arachidonic acid- and collagen-induced platelet aggregation were calculated to be 9.0 +/- 1.1 and 58.9 +/- 0.9 microM, respectively. Thromboxane B2 and prostaglandin D2 formation in platelets caused by arachidonic acid were also suppressed. Clausine-D inhibited increased intracellular concentration of calcium in platelets caused by arachidonic acid and collagen, and also abolished the generation of inositol monophosphate caused by arachidonic acid, but not that by collagen, U46619, PAF and thrombin. In human citrated platelet-rich plasma, clausine-D inhibited the secondary phase, but not the primary phase, of aggregation induced by epinephrine and ADP. These results indicate that the antiplatelet effect of clausine-D is due to inhibition of the formation of thromboxane A2.
克劳辛-D浓度依赖性地抑制花生四烯酸和胶原诱导的洗涤兔血小板的聚集和释放反应，而不影响U46619、PAF和凝血酶诱导的反应。克劳辛-D对花生四烯酸和胶原诱导的血小板聚集的IC50值分别计算为9.0±1.1和58.9±0.9微摩尔。花生四烯酸引起的血小板中血栓素B2和前列腺素D2的形成也受到抑制。克劳辛-D抑制花生四烯酸和胶原引起的血小板细胞内钙浓度升高，并且还消除了花生四烯酸引起的肌醇单磷酸的生成，但不消除胶原、U46619、PAF和凝血酶引起的生成。在人枸橼酸化富血小板血浆中，克劳辛-D抑制肾上腺素和ADP诱导的聚集的第二相，但不抑制第一相。这些结果表明，克劳辛-D的抗血小板作用是由于抑制血栓素A2的形成。
