In vitro inhibition of the activation of the human complement and coagulation systems by chloroquine.
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.
D000818:Animals; D000936:Antigen-Antibody Complex / Q000276:immunology; D001777:Blood Coagulation / Q000187:drug effects*; D002738:Chloroquine / Q000494:pharmacology*; D003167:Complement Activation / Q000187:drug effects*; D004305:Dose-Response Relationship, Drug; D006461:Hemolysis / Q000187:drug effects; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology; D066298:In Vitro Techniques; D011817:Rabbits; D015054:Zymosan / Q000494:pharmacology
D000936:Antigen-Antibody Complex; D007074:Immunoglobulin G; D002738:Chloroquine; D015054:Zymosan