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目的 :研究血小板蛋白激酶 C(PKC)在急性心肌梗塞 (AMI)中的活性 ,以揭示 PKC的致病机制。 方法 :利用 P-磷酸二氢钠标记血小板 ,以 PKC的底物 40 KD蛋白的磷酸化为酶激活的标志 ,对 AMI组及对照组PKC的基础活性及反应活性进行检测。经 t检验进行分析比较 ,同时检测两组的血小板数及血小板膜表面 α颗粒膜蛋白140 (GMP- 140 )分子数。 结果 :AMI组 PKC基础活性及经凝血酶刺激后的反应活性均较对照组显著增高 (P<0 .0 5 ) ;血小板膜表面 GMP-140水平较对照组显著增高 (P<0 .0 1)。 结论 :AMI中血小板 PKC的异常活化及高反应活性提示它在血栓形成中起重要作用
PURPOSE: To study the activity of platelet protein kinase C (PKC) in acute myocardial infarction (AMI) to reveal the pathogenesis of PKC. Methods: The basal activity and reactivity of PKC in AMI group and control group were detected by phosphorylation of 40 KD phosphorylation of PKC as a marker of enzyme activation by using P-sodium dihydrogen phosphate labeled platelets. The t-test was used to analyze and compare the number of platelets and the number of alpha-granule membrane protein 140 (GMP-140) on the platelet membrane. Results: The basal activity of PKC in AMI group and the activity of PKC after thrombin stimulation were significantly higher than those in control group (P <0.05). The level of GMP-140 on platelet membrane surface was significantly higher than that of control group (P <0.01) ). CONCLUSIONS: Abnormal activation and high reactivity of platelet PKC in AMI suggest that it plays an important role in thrombosis