中文摘要：

目的 探讨Toll样受体2（TLR2）在血小板激活及免疫方面的作用.方法 取健康人（n=5）全血6 ml,以密度梯度离心法制备洗涤血小板.用1、5、10μg/ml的TLR2激动剂Pam3CSK4（一种合成的细菌脂蛋白）刺激人洗涤血小板,然后测定血小板聚集率,血小板表面蛋白CD62p和TLR2表达的变化.结果 Pam3CSK4以浓度0、1、5和10μg/ml激活血小板：聚集率增加分别为（12.83±2.43）%、（28.32±5.67）%、（52.56±8.54）%、（76.24±11.23）%,P〈0.01;血小板表面CD62p表达量增加分别为（11.20±1.67）%、（18.45±2.66）%、（22.45±2.04）%、（29.53±4.08）%,P〈0.01.Pam3CSK4在1μg/ml时TLR2表达为（16.85±6.10）%,与对照组（10.81±3.99）%相比差异无统计学意义（P〉0.05）,在5 μg/ml、10μg/ml时TLR2表达量分别为（21.15±9.90）%和（22.52±9.26）%,与对照组比较差异有统计学意义（P〈0.05）.结论 细菌脂蛋白Pam3CSK4通过激活TLR2引起血小板聚集、活化,是血小板参与抑制革兰阳性细菌感染的免疫应答机制之一.

英文摘要：

Objective To investgate role of TLR2 in the activation, the innate immune and inflammation of human platelets. Methods Human washed platelets were separated from healthy people（n=5） and were stimulated with different concentrations（1μg/ml, 5μg/ml, 10μg/ml） of TLR2 agonistPam3CSK4（a synthetic bacterial lipoproteins）. Then the platelet aggregation rate, the expression of CD62p and TLR2 on the platelet surface were measured. Results The platelet aggregation rate were （28.32±5.67）%, （52.56±8.54）% and （76.24±11.23）%, respectively, at concentration of 1μg/ml, 5μg/mland 10μg/ml of Pam3CSK4, more than （12.83±2.43）% at 0μg/ml of it. In addition, the expression of CD62p were （18.45±2.66）%, （22.45±2.04）%, （29.53±4.08）%, respectively at above concentration of Pam3 CSK4, more than （11.20±1.67）% of CD62p at control group（P〈0.01）. The expression of TLR2 was not significantly increased at a lower concentration of Pam3CSK4（1μg/ml） with （16.85±6.10）% compared with（10.81±3.99）% at the control group. However, it were （21.15±9.90）% and （22.52±9.26）%, respectively, at a higher concentration（5μg/ml, 10μg/ml）more than（10.81±3.99）% at the control group（P〈0.05）. Conclusion Pam3CSK4 induce aggregation, activation and the up-regulation of TLR2 of platelet by stimulating TLR2 receptor of it. Thereafter, TLR2 play an important role in the innate immune of platelet.