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冠心病活化血小板内TFPI的表达及低分子肝素对其抗凝机制的作用 被引量:2

Expression of Tissue Factor Pathway Inhibitor(TFPI)mRNA in activated platelet in coronary heart disease(CHD) and the anticoagulant mechanism of low molecular weigh heparin(LMWH)for them
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摘要 目的探讨冠心病患者活化血小板内组织因子途径抑制剂(TFPI)的表达及其与低分子肝素(LMWH)抗凝机制的关系。方法用RT-PCR和ELASA法对急性心肌梗死(AMI)、不稳定型心绞痛(UA)、稳定型心绞痛(SA)患者及正常对照组(CG)进行血小板内TFPI水平和mRNA及三组患者应用LMWH前后血浆游离组织因子途径抑制剂(FTFPI)水平的检测。结果 (1)AMI组、UA组血小板内TFPI mRNA的表达升高,与对照组比较,差异有统计学意义(P<0.05)。(2)AMI组、UA组和SA组的FTFPI水平分别为93.39、74.91、62.98μg/L,与对照组相比,前两组水平明显升高。(3)血小板TFPI mRNA的表达与AMI组、UA组、SA组血浆FTFPI水平具有良好的相关性。(4)三组患者应用LMWH后,FTFPI水平分别为141.87、116.82、107.28μg/L,与治疗前相比,差异有统计学意义(P<0.01)。结论冠心病患者活化血小板内TFPI mRNA的表达升高,并且血小板内TFPI参与LMWH的抗凝机制。 Objective To investigate the expression of TFPI mRNA in activated platelet in CHD and the anticoagulant mechanism of LMWH for them. Methods By means of RT - PCR method and ELASA technique,the activated pletelet mRNA levels and the levels of free -TFPI were measured in patient with stable angina (SA) group,unstable angina (UA) , acute myocardial infarction (AMI) and control group in the study. Results ( I ) The mRNA expression level of TFPI in platelet were signifeieant higher in patient with AMI and UA than tbat of healthy survey( P 〈 0. 05 ). (2) Contrasting to the control group, the level of free - TFPI in patient with AMI or UA were significantly higher ( P 〈 0.01 ). The average level of FTFPI of those three groups were 93.39,74. 91 and 62.98 μg/L. (3)There were positive correlation between the mRNA expression of TFPI in platelet and the change of plasma free -TFPI in patients with AMI,UA and SA. (4)After the treatment by LMWH, free - TFP1 increased significantly among the AMI,UA and SA group. The average level of FTFPI of those three groups exposured to LMWH were 93.39,74.91 and 62.98μg/L. Conclusion The expression of TFPI were enhanced in CHD patient owing to platelet activation. TFPI were released from the pool of platelet into circulation when exposure to LMWH.
出处 《中国医学创新》 CAS 2010年第9期1-3,共3页 Medical Innovation of China
关键词 冠心病 血小板 低分子肝素 组织因子途径抑制剂 Coronary heart disease Platelet Low molecular weigh heparin TFPI
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  • 1唐雪元,郑兰香,赖少娟,李红卫,王建辉,李昕.脑梗死患者组织因子途径抑制物C-399T多态性[J].中华血液学杂志,2006,27(9):640-642. 被引量:2
  • 2TAPSON V F,CARROLL B A,DAVIDSON B L,et al. The diagnostic approach to acute venous thromboembolism. Clinical practice guideline. American Thoracic Society[J]. Am J Respir Crit Care Med, 1999, 160:1044-- 1066.
  • 3MOATTI D, HAIDAR B,FUMERON F,et al. A new T-287 polymorphism in the 5' regulatory region of the tissue factor pathway inhibitor gene association study of the T-287C and C-399T polymorphisms with coronary artery disease and plasma TFPI levels[J].Thromb Haemost, 2000,84 : 244-- 249.
  • 4SCHAFER A I,LEVINE M N,KONKLE B A,et al. Thrombotic disorder: diagnosis and treatment [J]. Hematol,2003,520-- 539.
  • 5LOPEZ J A, KEARON C, LEE A Y. Deep venous thrombosis[J]. Hematol Am Soc Hematol Educ Program, 2004,439-- 456.
  • 6European Society of Cardiology. Guidelines on diagnosis and management of acute pulmonary embolism[J]. Eur Heart J, 2000,21 : 1301 -- 1336.
  • 7BAJAJ M S,BIRKTOFT I J,STEER S A,et al. Structure and biology of tissue factor pathway inhibitor[J]. Thromb Haemost,2001,86: 957--972.
  • 8MIYALA T,SAKATA T,KUNEDA K,et al. C-399T polymophism in the promoter region of human tissue factor pathway inhibitor TFPI gene does not change the plasma TFPT antigen level and does not cause venous thrombosis[J]. Thromb Haemost, 1998,80 : 345 --346.
  • 9MOATTI D, SEKNADJI P, CALAND C, et al. Polymorphisms of the tissue factor pathway inhibitor (TFPI) gene in patients with acute coronary syndromes and in healthy subjects: impact of the V264M substitution on the plasma levels of TFPI. Arterioseler[J]. Thromb Vase Biol, 1999,19 : 862 -- 869.
  • 10Nadir Y, Vlodavsky I, Brenner B. Heparanase, tissue factor, and cancer[ J]. Semin Thromb Hemost, 2008, 34 (2) : 187- 194.

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