Ko F N, Yeh L J, Liang H C, Kuo S C, Teng C M
Pharmacological Institute, College of Medicine, National Taiwan University, Taipei.
J Pharm Pharmacol. 1996 Apr;48(4):395-400. doi: 10.1111/j.2042-7158.1996.tb05940.x.
p-Chlorobiphenyl (1-50 microM) concentration-dependently 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 and thrombin. The IC50 values of p-chlorobiphenyl on the arachidonic acid and collagen-induced platelet aggregation were 2.9 +/- 0.5 and 12.8 +/- 2.3 microM, respectively. The formation of both platelet thromboxane B2 and prostaglandin D2 caused by arachidonic acid was inhibited by p-chlorobiphenyl concentration-dependently. In myo-[3H]inositol-labeled and fura-2-loaded platelets. [3H]inositol monophosphate generation and the rise in intracellular Ca2- stimulated by arachidonic acid were inhibited by p-chlorobiphenyl. In human platelet-rich plasma, p-chlorobiphenyl and indomethacin prevented the secondary aggregation and blocked ATP release from platelets induced by adenosine 5'-diphosphate and adrenaline without affecting the primary aggregation. It is concluded that p-chlorobiphenyl may be a cyclo-oxygenase inhibitor and its antiplatelet action is mainly due to the inhibition of thromboxane formation.
对氯联苯（1 - 50微摩尔）呈浓度依赖性地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和凝血酶诱导的反应。对氯联苯对花生四烯酸和胶原诱导的血小板聚集的IC50值分别为2.9±0.5和12.8±2.3微摩尔。对氯联苯呈浓度依赖性地抑制花生四烯酸引起的血小板血栓素B2和前列腺素D2的形成。在肌醇-[3H]标记和fura - 2负载的血小板中，对氯联苯抑制花生四烯酸刺激的[3H]肌醇单磷酸生成和细胞内Ca2+升高。在富含人血小板的血浆中，对氯联苯和吲哚美辛可防止由5'-二磷酸腺苷和肾上腺素诱导的血小板继发性聚集并阻止ATP释放，而不影响原发性聚集。结论是对氯联苯可能是一种环氧化酶抑制剂，其抗血小板作用主要是由于抑制血栓素的形成。
