摘要
目的 :研究脂蛋白 (a) [L p(a) ]在血小板血栓形成中的作用及其机制。方法 :以 32 P- Na H2 PO4标记正常健康者的血小板 ,观察加入 L p(a)后血小板蛋白激酶 C(PKC)底物 47kd蛋白磷酸化反应情况 ,并设空白对照 ,比较L p(a)对血小板 PKC活性的影响。结果 :随着加入的 L p(a)浓度不断增高 ,血小板 PKC底物 47kd蛋白磷酸化程度也随之不断增强 ,即 L p(a)终浓度分别为 0 ,0 .0 83,0 .16 5 ,0 .33,0 .5 5 m g/ m l时 ,磷酸化反应后的光密度值分别为6 2 5 .0 0、180 8.0 0、2 0 39.46、5 2 5 9.83、6 842 .6 3;加入一定终浓度 (0 .16 5 m g/ ml)的 L p(a)后 ,其磷酸化反应程度随反应时间的延长而增强 ,即在 0 ,1,3,10 ,30 min反应时 ,磷酸化反应后的光密度值分别为 5 14.13、116 8.33、132 5 .0 0、3416 .0 0、12 139.0 0。结论 :L p(a)促进血小板 PKC底物 47kd蛋白磷酸化 ,从而增强血小板 PKC的活性 ,活化血小板 ,促进早期血栓形成。
Objective: Our purpose was to study the effect and mechanism of Lp(a) on platelet thrombosis. Methods: We labelled platelet of healthy individuals with 32 P NaH 2PO 4 and observed the degree of phosphorylation of the 47 kd substrate of PKC in platelet. The effect of Lp(a) on the activity of protein kinase C (PKC) in platelet was compared with the control. Results: With the gradual increase of the concentration of Lp(a), the degree of phosphorylation of the 47 kd substrate of PKC in platelet gradually increased, too. When the final concentrations of Lp(a) were 0, 0.083, 0.165, 0.33, 0.55 mg/ml, the scanning values of phosphorylation of 47 kd substrate of PKC were 625.00, 1808.00, 2039.46, 5259.83, 6842.63, respectively. When the final concentration of Lp(a) was 0.165 mg/ml, with the gradual extension of time, the degree of phosphorylation of the 47 kd substrate of PKC gradualey increased. At 0, 1, 3, 10, 30 min, the scanning values of phosphorylation of 47 kd substrate of PKC were 514.13, 1168.33, 1325.00, 3416.00, 12139.00, respectively. Conclusion: Lipoprotein(a) can accelerate phosphorylation of the 47 kd substrate of PKC in platelet, sequentially increase the activity of PKC. It can activate platelet thrombosis.
出处
《中国医科大学学报》
CAS
CSCD
北大核心
2000年第5期382-384,共3页
Journal of China Medical University
基金
辽宁省自然科学基金!资助项目 96 2 2 89
