Sak衍生体对高血脂大鼠血小板功能的影响及其作用机制

目的: 观察Sak衍生体对高血脂大鼠血小板功能的影响并探讨其作用机制。方法: 30只Wistar大鼠制备高脂大鼠模型，随机分为药物组、高脂组及正常对照组。药物组大鼠尾静脉注射Sak衍生体进行干预，剂量为0.5 mg?kg-1，隔天注射，共15次；其他两组大鼠注射生理盐水作为对照，在给药前和最后一次给药24 h后采血，检测各组大鼠的血小板黏附率和二磷酸腺苷二钠(ADP)诱导的血小板聚集率；采用放免法检测血小板中钙调蛋白(CaM)含量以及ADP诱导的血小板聚集时血栓素(TXA2)的释放量。结果:与高脂组大鼠比较，药物组高脂大鼠血小板黏附功能及ADP诱导的血小板聚集率明显降低（分别是63.5%±6.71%与44.7%±8.13%，P<0.05；91.56%±9.01%与81.22%±3.45%，P<0.05），血小板中CaM含量与TXA2的释放量明显降低（P<0.05或P<0.01）。结论:Sak衍生体通过对引起血小板活化途径的干预，抑制血小板的黏附及聚集。

Effect of Sak deveration on function of platelets in hyperlipemia rats and its mechanism

Objective To study the effect of staphylokinase derivation (SakD) on the function of platelet in hyprlipemia rats and its mechanism. Methods 30 Wistar rats were randomly divided into 3 group:SakD group,hyperlipemia group and normal diet group (n=10). The rats in SakD group received SakD i.v. for 15 times (0.5 mg·kg-1,once every other day) respectively,and the rats in other two groups received normal saline in the same way after 8 weeks feeding. The blood samples were collected before administration and 24 h after the last injection. Then the platelet adhesion rate and the adenosine diphosphate(ADP)-induced platelet aggregation rates in various groups were detected,the contents of calmodulin (CaM) and thromboxane(TXA2)in platelet were measured with radioimmunoassay. Results Compared with hyperlipemia group,the adhesion platelet function and ADP-induced platelet aggregation of hyperlipemia rats in SaKD group was significantly decreased(63.5%±6.71% and 44.7%±8.13%,respectively,P<0.05;91.56%± 9.01% and 81.22%±3.45%,P<0.05),the releasing of platelet TXA2 and CaM content in platelet were significantly reduced (P<0.05 or P<0.01) Conclusion SakD can suppress the platelet agglutination and adhesion by intervention of different pathways of platelet activation.