Skrha J, Hodinár A, Kvasnicka J, Hilgertová J
Department of Internal Medicine 3, Faculty of Medicine 1, Charles University, Prague, Czech Republic.
Diabet Med. 1996 Sep;13(9):800-5. doi: 10.1002/(SICI)1096-9136(199609)13:9<800::AID-DIA178>3.0.CO;2-Q.
This study attempted to verify the existence of a relationship between oxidative stress documented by malondialdehyde (MDA) and superoxide dismutase (SOD) and fibrinolysis analysed by tissue plasminogen activator (tPA) and its inhibitor (PAI-1) in diabetes mellitus. Forty-seven patients with Type 1 (n = 27) and Type 2 (n = 20) diabetes were examined together with 20 non-diabetic controls. The following were analysed: plasma MDA concentration, SOD activity in erythrocytes, tPA activity and antigen, PAI-1 activity and antigen, fasting blood glucose, fructosamine, glycated haemoglobin (HbAlc), and urine albumin. SOD activity was decreased in patients with diabetes. This contrasted with an increased plasma MDA concentration especially in Type 2 diabetes as compared with Type 1 or healthy persons (p < 0.001). tPA activity was increased in both groups of patients with diabetes as compared to healthy persons (p < 0.001), PAI-1 activity was higher in Type 2 diabetes with vascular changes than in the remaining subgroups (p < 0.001). Multivariate analysis revealed a significant positive relationship between plasma MDA concentrations and PAI-1 antigen (r = 0.53, p < 0.001) and a negative relationship between SOD and tPA activities (r = -0.53, p < 0.01). We conclude that oxidative stress may modulate fibrinolytic properties in diabetes mellitus.
本研究试图验证糖尿病患者中,由丙二醛(MDA)和超氧化物歧化酶(SOD)记录的氧化应激与通过组织纤溶酶原激活物(tPA)及其抑制剂(PAI-1)分析的纤维蛋白溶解之间是否存在关联。对47例1型糖尿病患者(n = 27)和2型糖尿病患者(n = 20)以及20名非糖尿病对照者进行了检查。分析了以下指标:血浆MDA浓度、红细胞中的SOD活性、tPA活性和抗原、PAI-1活性和抗原、空腹血糖、果糖胺、糖化血红蛋白(HbAlc)以及尿白蛋白。糖尿病患者的SOD活性降低。这与血浆MDA浓度升高形成对比,尤其是2型糖尿病患者与1型糖尿病患者或健康人相比(p < 0.001)。与健康人相比,两组糖尿病患者的tPA活性均升高(p < 0.001),有血管病变的2型糖尿病患者的PAI-1活性高于其余亚组(p < 0.001)。多变量分析显示血浆MDA浓度与PAI-1抗原之间存在显著正相关(r = 0.53,p < 0.001),SOD与tPA活性之间存在负相关(r = -0.5)。我们得出结论,氧化应激可能调节糖尿病患者的纤维蛋白溶解特性。