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AIM: To investigate the effects of copper-aspirin complex on rat thrombosis and the interaction between plateletsand neutrophils. METHODS: The model of electrically stimulated carotid artery thrombosis in Sprague Dawleyrats was used; the effects of copper-aspirin complex on rat platelet-neutrophil adhesion and platelet aggregationstimulated by activated neutrophils were observed by rosette assay and Borns method, respectively. RESULTS:Intragastric copper-aspirin complex (5, 7, and 10 mg/kg) dose-dependently prolonged the occlusion time; it signifi-cantly decreased the rosette number formed between thrombin-activated platelets and neutrophils; the 50 % ofinhibitory concentration (IC50) was (54.64.3) mol/L. Copper-aspirin complex markedly inhibited rat plateletaggregation induced by either cell free supernatant of activated neutrophils or by activated neutrophil suspension.The values of IC50 were (224.516.2) mol/L and (820.521.4) mol/L, whereas aspirin had no influence.CONCLUSION: Copper-aspirin complex inhibited platelet-neutrophil interactions through a different property fromaspirin and resulted in a more potent antithrombotic activity.
A: To investigate the effects of copper-aspirin complex on rat thrombosis and the interaction between platelets and neutrophils. METHODS: The model of electrically stimulated carotid artery thrombosis in Sprague Dawleyrats was used; the effects of copper-aspirin complex on rat platelet-neutrophil adhesion and platelet aggregationstimulated by activated neutrophils were observed by rosette assay and Borns method, respectively. RESULTS: Intragastric copper-aspirin complex (5, 7, and 10 mg / kg) dose-dependently prolonged the occlusion time; it signifi-cantly decreased the rosette The 50% of inhibitor concentration (IC50) was (54.64.3) mol / L. Copper-aspirin complex markedly inhibited rat plate letaggregation induced by either cell free supernatant of activated neutrophils or by activated neutrophil suspension . The values of IC50 were (224.516.2) mol / L and (820.521.4) mol / L, asp aspirin had no influence. CONCLUSION: Cop per-aspirin complex inhibited platelet-neutrophil interactions through a different property fromaspirin and resulted in a more potent antithrombotic activity.