急性脑梗死患者血浆尿激酶型纤溶酶原激活物及其受体的表达

Expression of urokinase-type plasminogen activator and its receptor in plasma of patients with cerebral infarction

目的 检测急性脑梗死患者血浆中尿激酶型纤溶酶原激活物 (uPA)及其受体 (uPAR)的含量变化 ,并探讨其在脑梗死发生发展过程中的作用。方法 应用ELISA双抗体夹心法分别测定89例急性脑梗死患者、30例其他疾病对照组和 30名健康对照组血浆中uPA和uPAR含量 ,并按病情分轻、中、重 3组进行比较。结果 脑梗死患者急性期血浆uPA和uPAR含量分别为 ( 16 6 4± 384 )ng/L及 ( 1375± 30 3)ng/L ,其他疾病对照组为 ( 10 33± 12 3)ng/L及 ( 978± 12 0 )ng/L ,正常对照组为 ( 10 0 5±12 9)ng/L及 ( 90 5± 15 9)ng/L。脑梗死组与后两组比较P <0 0 5或P <0 0 1。脑梗死患者恢复期uPA含量为 ( 1186± 385 )ng/L ,与两对照组比较P >0 0 5 ,uPAR含量为 ( 115 9± 2 6 1)ng/L ,明显高于两对照组 (均P <0 0 1)。重度患者急性期血浆uPA和uPAR含量分别为 ( 1939± 2 5 7)ng/L及 ( 15 11± 379)ng/L ,中度患者分别为 ( 15 94± 2 0 5 )ng/L及 ( 12 97± 15 1)ng/L ,轻度患者分别为 ( 135 9± 176 )ng/L及 ( 12 2 7± 98)ng/L ,重度患者组与后两组比较P <0 0 1;恢复期uPA和uPAR含量分别为 ( 115 3± 170 )ng/L及( 1186± 15 8)ng/L ,轻度患者分别为 ( 10 4 2± 187)ng/L及 ( 10 5 4± 10 9)ng/L ,两者比较P <0 0

Objective To measure the urokinase type plasminogen activator (UPA) and its receptor (UPAR) in the plasma of patients with cerebral infarction and to study the effects of UPA and UPAR on cerebral infarction. Methods ELISA sandwich method was used to measure the plasma levels of UPA and UPAR in 89 patients with acute cerebral infarction, subdivided into mild, moderate and severe subgroups according to the modified Edinburgh Scandinavia stroke scale (mESSS), and 30 patients with other disease and 30 healthy persons as controls. Results Within 2 days after the onset of cerebral infarction the UPA and UPAR levels were (1663.7±384.2) ng/L and (1 375.3±303.0) ng/L respectively, both significantly higher than those of the patients with other diseases [(1 033.0±122.7) ng/L and (978.3±120.0) ng/L respectively ( P =0.038 and P =0.000)] and those of the normal control group [(1 005.0±128.9) ng/L and (904. 7±158.6) ng/L respectively, both P =0.000]. Two weeks after the onset of stroke, the plasma UPA level was (1 185.5±384.6) ng/L, not significantly different from those of the 2 control groups (both P >0.05); while the plasma UPAR level in the cerebral infarction was (1 159.3±261.2) ng/L, significantly higher than those in the 2 control groups ( P <0.01). Within 2 days after the onset of infarction the plasma UPA and UPAR levels of the severe subgroup were (1 938.9±256.5) ng/L and (1 510.8±378.7) ng/L respectively, both significantly higher than those of the moderate subgroup [(1 593.7±204.8) ng/L and (1 296.6±151.2) ng/L respectively, both P <0.01] and those of the mild subgroup [1 358.5±175.9] ng/L and (1 226.8±98.3) ng/L respectively, both P <0.01], Two weeks after the onset of stroke,the plasma UPA and uPAR levels of the severe subgroup remained significantly higher than those of the mild subgroup [(1 152.6±170.3) ng/L vs (1 041.9±187.0) ng/L, ( P <0.05)] and [(1 186.4±158.3) ng/L vs (1 053.9±109.4) ng/L ,( P <0.01)]. In addition, the plasma UPA and UPAR levels of the patients who died from cerebral infarction at last were the highest among all the groups. Conclusion The plasma levels pf UPA and UPAR increase in patients with cerebral infarction and may be related with the severity of disease. The UPA and UPAR genes may play an important role via proteolytic degradation of the extracellular matrix and basement membrane during the development of cerebral infarction.