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2型糖尿病患者t-PA、PAI-1水平及胰激肽原酶治疗后的变化

孙超,尹晓,蒲迎,孙金凤   

  1. 山东大学附属济南市中心医院内分泌科, 济南 250013
  • 收稿日期:2008-07-22 修回日期:1900-01-01 出版日期:2008-11-16 发布日期:2008-11-16
  • 通讯作者: 孙超

Plasma t-PA and PAI-1 levels in patients with type 2 diabetes and the effect of pancreatic kallikrein

SUN Chao, YIN Xiao, PU Ying, SUN Jin-feng   

  1. Department of Endocrinology and Metabolism, Jinan Central Hospital Affiliated to Shandong University, Jinan 250013, China
  • Received:2008-07-22 Revised:1900-01-01 Online:2008-11-16 Published:2008-11-16
  • Contact: SUN Chao

摘要: 目的测定2型糖尿病患者纤溶酶原激活物(t-PA)、纤溶酶原激活抑制物-1(PAI-1)水平,并观察胰激肽原酶治疗后的变化。方法选取2型糖尿病患者88例,分为无血管并发症组和有血管并发症组,另设正常对照组,测量身高、体质量、血压、血糖、血脂等指标,用酶联免疫吸附双抗体夹心法(ELISA)测定胰激肽原酶治疗前后血浆t-PA、PAI-1水平。结果两组糖尿病患者t-PA水平均低于正常对照组,PAI1水平均高于正常对照组(P<0.05或0.01);有血管并发症组tPA水平低于无血管并发症组,PAI1水平高于无血管并发症组(P均<0.01)。t-PA与TG、LDL-C呈负相关(P<0.01),PAI-1与BMI、SBP、FBG、HbA1c、TG、LDL-c呈正相关(P<0.01),与HDL呈负相关(P<0.01)。两组糖尿病患者用胰激肽原酶治疗后,PAI-1水平下降,t-PA水平升高。结论糖尿病患者血浆t-PA水平降低,PAI-1水平升高,尤其是伴有血管并发症者变化更明显,胰激肽原酶治疗后,可改善t-PA和PAI-1水平的异常变化。

关键词: 纤溶酶原激活物抑制物, 胰激肽原酶, 非胰岛素依赖型, 纤溶酶原激活剂, 糖尿病

Abstract: To investigate the relationship of chronic diabetic vascular complication and plasma t-PA and PAI-1 levels in type 2 diabetes and the effect of pancreatic kallikrein(TPK)on them. Methods88 patients with type 2 diabetes and 30 healthy controls were recruited into the study. Plasma t-PA and PAI-1 levels were determined by ELISA. Measurements were also carried out before and after the interfered treatment of TPK. ResultsCompared with the healthy controls, the diabetes patients showed a decreased plasma t-PA level and an increased PAI-1 level (P<0.05 or<0.01). The plasma t-PA level in diabetes patients with vascular complications was lower and the PAI-1 level was higher than those without vascular complications (both P<0.01). The plasma t-PA level increased and the PAI-1 level decreased in diabetes patients after the treatment of TPK. tPA had a negative relationship with plasma TG and LDL-c levels, and PAI-1 had positive relationships with BMI, plasma TG and LDL-c levels, FBG, SBP and HbA1c. ConclusionPlasminogen dysfunction is an essential factor in the occurrence and development of diabetic vascular complications. The interfered treatment of TPK may prevent the development of type 2 diabetes and its vascular complications.

Key words: Type 2 diabetes, Tissue plasminogen activator, Plasminogen activator inhibitor-1, Pancreatic kallikrein

中图分类号: 

  • R587.2
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