摘要
目的探讨脑梗死患者阿司匹林抵抗与血小板环氧合酶2(cyclooxygenase-2,COX-2)的关系。方法 95例脑梗死患者服用阿司匹林(100mg/d)14d后,用二磷酸腺苷(adenosine phosphate,ADP)和花生四烯酸(arachidonic acid,AA)作诱导剂,测定血小板最大聚集率,并通过测定其尿11-脱氢-血栓素B2(11-dehydrothromboxane B2,11-dh-TXB2)的水平观察体内阿司匹林对血小板功能的抑制程度(11-dh-TXB2≤1500pg/mg判定为阳性),同时用蛋白质印迹技术检测了血小板COX-2的表达水平。结果脑梗死患者阿司匹林抵抗和半抵抗的发生率为27.4%,阿司匹林抵抗组尿11-dh-TXB2水平比敏感组显著升高(P<0.001),而阳性率显著降低(P<0.001),血小板COX-2表达明显增多。结论血小板COX-2可能参与了脑梗死患者阿司匹林抵抗的发生机制。
Objective To evaluate the relationship of platelet cyclooxygenase-2 and aspirin resistance in patients with cerebral infarction. Methods The whole blood platelet aggregation under arachidonic acid （AA） and adenosine phos- phate （ADP） stimulation and urine levels of 11-dehydrothromboxane B2 normalized to urinary creatinine were assessed in 95 patients with cerebral infarction after a 14-day period of aspirin intake at a daily dose of 100mg. Simultaneously cyclooxy- genase-2 expression in platelets was investigated by Western blot. Results Aspirin resistance and aspirin semi-resistance was found in 26 （27.4%） patients. Urine levels of 11-dehydrothromboxane B2 in AR patients were signifcantly higer than those in aspirin sensitive patients （ P 〈 0. 001 ）. COX-2 expression in platelets of AR patients was obviously upregulated. Conclusion Platelet COX-2 might partially account for aspirin resistance in patients with cerebral infarction and the exact mechanism of AR remains further evaluation.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2012年第6期490-492,共3页
Journal of Apoplexy and Nervous Diseases
