Teng C M, Lee L G, Lee C Y, Ferlan I
Pharmacological Institute, College of Medicine, National Taiwan University, Taipei, Taiwan, R.O.C.
Thromb Res. 1988 Dec 1;52(5):401-11. doi: 10.1016/0049-3848(88)90024-2.
Equinatoxin, isolated from Actinia equina, caused aggregation of washed rabbit platelets at a concentration as low as 0.01 ng/ml. ATP was released, but no formation of thromboxane B2 in challenged platelets. The aggregation was resistant to indomethacin or creatine phosphate/creatine phosphokinase or PAF antagonist. The aggregation was inhibited by imipramine, sodium nitroprusside, mepacrine, theophylline, prostaglandin E1 and EDTA. However, heparin and tetracaine were without any inhibitory effect. Verapamil suppressed both the aggregation and release reaction caused by equinatoxin in calcium concentrations from 0.01 to 15 mM. High concentrations of equinatoxin caused progressive cell lysis. It is concluded that equinatoxin-induced platelet aggregation is independent of ADP, thromboxane or PAF pathway. Phosphoinositide breakdown by phospholipase C is postulated to accomplish this phospholipase A2-independent platelet aggregation by equinatoxin.
从海葵中分离出的海葵毒素，在低至0.01纳克/毫升的浓度下就能引起洗涤过的兔血小板聚集。会释放出ATP，但在受到刺激的血小板中不会形成血栓素B2。这种聚集对吲哚美辛、磷酸肌酸/肌酸磷酸激酶或血小板活化因子拮抗剂有抗性。这种聚集可被丙咪嗪、硝普钠、米帕林、茶碱、前列腺素E1和乙二胺四乙酸抑制。然而，肝素和丁卡因没有任何抑制作用。维拉帕米在0.01至15毫摩尔的钙浓度下能抑制海葵毒素引起的聚集和释放反应。高浓度的海葵毒素会导致细胞逐渐裂解。得出的结论是，海葵毒素诱导的血小板聚集独立于ADP、血栓素或血小板活化因子途径。推测磷脂酶C引起的磷酸肌醇分解通过海葵毒素实现这种不依赖磷脂酶A2的血小板聚集。
