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目的 探讨老年急性脑梗死患者脂蛋白 ( a)〔Lp( a)〕及血小板蛋白激酶 C( PKC)的变化及相互关系。 方法 检测 3 0例老年急性脑梗死患者 Lp( a)水平及血小板膜相对分子质量 4 70 0 0、2 0 0 0 0蛋白质表达的 PKC活性 ,并设对照组。 结果 脑梗死组 Lp( a)水平〔中位数 ( M)为 3 3 4 .1 4mg/ L〕较对照组 ( 1 3 6.2 6mg/ L)显著升高 ( P<0 .0 1 ) ;血小板 PKC的基础活性 ( 0 min)、活化 3 min及1 0 min的活化活性 ,脑梗死组由相对分子质量为 4 70 0 0的膜蛋白质表达分别为 4 872、60 1 9及 74 52cpm,对照组分别为 2 0 1 5、2 886及 3 74 1 cpm;脑梗死组由相对分子质量为 2 0 0 0 0的膜蛋白质表达分别为 2 4 1 8、3 52 6及 4 42 3 cpm,对照组分别为 1 84 3、2 559及 3 0 2 2 cpm。梗死组较对照组均显著升高(均为 P<0 .0 1 ) ;Lp( a)与血小板 PKC存在正相关关系。 结论 高水平的 Lp( a)与异常活化的血小板 PKC是老年人急性脑梗死的重要致病因素 ,而 Lp( a)与血小板 PKC的活化有密切的关系。
Objective To investigate the changes and correlations of lipoprotein (a) [Lp (a)] and platelet protein kinase C (PKC) in elderly patients with acute cerebral infarction. Methods The PKC activity of Lp (a) in 30 elderly patients with acute cerebral infarction and protein expression of platelet membrane with a molecular weight of 4 700 0 200 000 was detected and compared. Results The level of Lp (a) in the infarction group was significantly higher than that of the control group (133.66 mg / L) (P <0.01) The basal activity of PKC (0 min), activated 3 min and activation activity of 10 min, the expression of membrane protein of 4 70 0 0 in the infarcted group were 4872, 6019 and 74 52 cpm, respectively. The control group Respectively, respectively. The protein expression of membrane proteins with relative molecular mass of 200 000 in cerebral infarction group were respectively 2 148, 526 and 42 42 cpm, while in control group Respectively 1 843, 2 559 and 302 2 cpm. Infarction group than the control group were significantly increased (P <0.01); Lp (a) and platelet PKC there is a positive correlation. Conclusions High levels of Lp (a) and abnormally activated platelet PKC are important causative factors in the elderly with acute cerebral infarction. Lp (a) is closely related to the activation of platelet.