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。
Objective To investigate the relationship of chronic diabetic vascular complication and plasma t-PA arid PAI-1 levels in type 2 diabetes and the effect of pancreatic kallikrein（TPK）on them. Methods 88 patients with type 2 diabetes and 30 healthy controls were recruited into the study. Plasma t-PA and PM-1 levels were determined by ELISA. Measurements were also carried out before and after the interfered treatment of TPK. Results Compared with the healthy controls, the diabetes patients showed a decreased plasma t-PA level and an increased PAl- 1 level （ P 〈 0.05 or 〈 0.01）. The plasma t-PA level in diabetes patients with vascular complications was lower and the PM-1 level was higher than those without vascular complications （both P 〈 0.01）. The plasma t-PA level increased and the PM-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 HbAlc. Conclusion Plasminogen 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.
出处
《山东大学学报（医学版）》
CAS
北大核心
2008年第11期1060-1062,共3页
Journal of Shandong University:Health Sciences
