Ramanathan V D, Sengupta U
Int J Immunopharmacol. 1985;7(5):769-73. doi: 10.1016/0192-0561(85)90164-x.
The ability of chloroquine to inhibit the activation of the complement and coagulation systems was investigated. The activation of the classical pathway of complement by antibody coated sheep erythrocytes and aggregated IgG was blocked by chloroquine. Similarly, it prevented normal rabbit erythrocytes and zymosan from activating the the alternative pathway of complement. The activation of C3 by immune complexes of different solubilities also was inhibited by this drug. In addition, it abrogated the clotting of plasma by calcium chloride and thrombin. This effect could be reversed by the addition of excess thrombin but not of calcium chloride. It is suggested that the inhibition of these two important phlogistic mediator systems of inflammation may contribute to the anti-inflammatory property of chloroquine.
研究了氯喹抑制补体和凝血系统激活的能力。抗体包被的绵羊红细胞和聚集的IgG对补体经典途径的激活被氯喹阻断。同样,它阻止正常兔红细胞和酵母聚糖激活补体替代途径。不同溶解度的免疫复合物对C3的激活也被该药物抑制。此外,它消除了氯化钙和凝血酶引起的血浆凝固。加入过量凝血酶可逆转这种效应,但加入氯化钙则不能。提示氯喹对炎症这两个重要的炎症介质系统的抑制作用可能有助于其抗炎特性。