摘要
目的探讨血小板膜糖蛋白(GP)Ⅰa C807T基因多态性与脑梗死急性期血小板功能的关系.方法应用聚合酶链反应-限制性片段长度多态性方法,检测147例脑梗死病人及120名正常对照者(对照组)的GPⅠa C807T基因型;体外应用Ⅰ型胶原诱导,比浊法检测血小板聚集;采用流式细胞仪测定外周血活化血小板分子标记物颗粒蛋白(GMP)CD62p、CD63表达.结果脑梗死组GPⅠa T等位基因频率高于对照组,差异有统计学意义(χ2=3.85,P〈0.05).对照组与脑梗死组T等位基因携带者加入胶原90 s时血小板聚集率较CC基因型者显著增高(t=7.4~9.9, P〈0.05),而两者最大血小板聚集率无显著性差异(t=1.19~1.30, P〉0.05).脑梗死组T等位基因携带者CD62p、CD63阳性率明显高于CC基因型者(t=10.3~17.8,P〈0.05).结论血小板膜GPⅠa T807等位基因可能是脑梗死的遗传危险因素,血小板功能增强可能是T等位基因促进脑梗死发病的机制之一.
Objective To investigate the association of the platelet glycoprotein Ⅰa C807 T gene polymorphism and the function of platelet in acute cerebral infarction. Methods By PCR-restrietion fragment length polymorphism technique, the platelet glycoprotein Ⅰa C807 T genotypes were detected in 147 patients with cerebral infarction and 60 healthy controls. Collagen type Ⅰ -induced platelet aggregation was measured by turbidimetry. A marker of activated platelet CD62p and CD63 was measured by whole blood flow cytometry. Results The frequencies of GP Ⅰa T allele were significantly higher in the infarction group than in the control one (x^2= 3.85, P〈0. 05). Collagen type Ⅰ-induced platelet aggregation was significantly higher in the individuals with GP Ⅰ a T allele than in those with CC genotype (t=7.4- 9.9, P〈0.05), but no significant difference was found in the maximal platelet aggregation between them (t=1.19-1.30, P〉0. 05). The expression of CD62p and CD63 was significantly higher in the cerebral infarction group with T allele than in CC genotype (t=10.3-17.8, P〈0. 05). Conclusion The platelet collagen receptor GPⅠa- Ⅱ a T807 allele might be an independent risk factor in the development of cerebral infarction. Enhanced platelet function might be one of the mechanisms of T allele in the pathogenesis of cerebral infarction.
出处
《齐鲁医学杂志》
2006年第2期111-113,共3页
Medical Journal of Qilu