Nosál R, Jancinová V, Petríková M
Institute of Experimental Pharmacology, Slovak Academy of Sciences, Bratislava.
Thromb Res. 1995 Mar 15;77(6):531-42. doi: 10.1016/0049-3848(95)00028-3.
Chloroquine inhibited arachidonic acid liberation from membrane phospholipids of thrombin- and A23187- stimulated platelets. In addition, it dose-dependently inhibited stimulated malondialdehyde formation and thromboxane B2 generation in the same platelets. The linear correlation between the inhibition of arachidonic acid liberation and malondialdehyde formation indicated that chloroquine inhibited activated phospholipase A2 in thrombin-stimulated platelets, similarly as it does in different cells and tissues. Yet, the nonlinear relationship between arachidonic acid liberation along with malondialdehyde formation and thromboxane generation as well as aggregation suggest that phospholipase A2 does not seem to be the only site of chloroquine action. Rather, it may affect platelets either at other levels of the arachidonic acid cascade too, or at some different stimulatory pathways, like intraplatelet calcium mobilisation, phosphoinositide cycle, calmodulin and protein kinase C activation.
氯喹抑制凝血酶和A23187刺激的血小板膜磷脂中花生四烯酸的释放。此外，它还能剂量依赖性地抑制相同血小板中刺激诱导的丙二醛形成和血栓素B2生成。花生四烯酸释放抑制与丙二醛形成之间的线性相关性表明，氯喹在凝血酶刺激的血小板中抑制活化的磷脂酶A2，这与它在不同细胞和组织中的作用类似。然而，花生四烯酸释放以及丙二醛形成与血栓素生成和聚集之间的非线性关系表明，磷脂酶A2似乎不是氯喹作用的唯一位点。相反，它可能在花生四烯酸级联反应的其他水平，或在一些不同的刺激途径，如血小板内钙动员、磷酸肌醇循环、钙调蛋白和蛋白激酶C激活等方面影响血小板。
