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目的探讨肝硬化患者血浆尿激酶型纤溶酶原激活物(uPA)、尿激酶型纤溶酶原激活物受体(uPAR)、纤溶酶原激活物抑制剂-1(PAI-1)变化及其意义。方法检查确诊的72例乙肝后肝硬化患者,依据Child-Pugh分级分为3级,其中A级23例,B级29例,C级20例。健康志愿献血者6例做为正常对照组。酶联免疫吸附法(ELISA)测定血浆uPA、uPAR、PAI-1的变化。同时检测血浆TGF-β1、透明质酸、Ⅲ型前胶原(PCⅢ)变化以及血浆白蛋白、胆红素、凝血酶原活动度改变。结果随着肝硬化的进展,血浆uPA、uPAR、PAI-1逐渐增加,血浆TGFβ1、血透明质酸、Ⅲ型前胶原也明显增加。Child C组患者血浆uPA、uPAR、PAI-1水平明显高于ChildA、ChildB组。Child A组PAI-1/uPA值下降,而Child B组、Child C组PAI-1/uPA又复升高。Child C组血浆uPA、uPAR、PAI-1水平与正常组、Child A组相比,差异显著。在Child A组,血浆uPA与PCⅢ呈负相关,与TGFβ1正相关;在Child C组血浆TGFβ1与血Ⅲ型胶原呈正相关,与HA呈正相关。结论血浆uPA、uPAR、PAI-1变化与肝硬化发生发展密切相关。肝硬化晚期,虽然血浆uPA、PAI-1增加,但总的效应表现为uPA相对不足,肝基质纤维降解受抑。适当增加uPA活性,抑制TGFβ1的早期激活,抑制肝硬化晚期PAI-1过度表达,可能有助于抑制HSC的激活、增加肝细胞外基质降解,从而有助于延缓肝硬化的发生发展。
Objective To investigate the changes of plasma urokinase-type plasminogen activator (uPA), urokinase-type plasminogen activator receptor (uPAR) and plasminogen activator inhibitor-1 (PAI-1) And its significance. Methods Totally 72 patients with posthepatitic cirrhosis who were diagnosed as HBV were divided into 3 grades according to Child-Pugh classification, including 23 cases of A grade, 29 cases of B grade and 20 cases of C grade. 6 healthy volunteer donors as normal control group. The changes of plasma uPA, uPAR and PAI-1 were measured by enzyme-linked immunosorbent assay (ELISA). At the same time, the changes of plasma TGF-β1, hyaluronic acid, type Ⅲ procollagen (PCⅢ) and the activities of plasma albumin, bilirubin and prothrombin were also detected. Results With the progress of liver cirrhosis, the levels of uPA, uPAR and PAI-1 in plasma gradually increased, and the levels of plasma TGFβ1, blood hyaluronic acid and type Ⅲ procollagen also increased significantly. The plasma levels of uPA, uPAR and PAI-1 in Child C group were significantly higher than those in ChildA and ChildB groups. PAI-1 / uPA values in Child A group decreased, while PAI-1 / uPA in Child B group and Child C group increased again. Child C group plasma uPA, uPAR, PAI-1 levels compared with the normal group, Child A group, the difference was significant. In Child A group, plasma uPA was negatively correlated with PCⅢ and positively correlated with TGFβ1. In Child C group, TGFβ1 was positively correlated with type Ⅲ collagen and positively correlated with HA. Conclusion The changes of plasma uPA, uPAR and PAI-1 are closely related to the occurrence and development of cirrhosis. Although the plasma levels of uPA and PAI-1 are increased in the late phase of liver cirrhosis, the overall effect is that uPA is relatively deficient, and liver fibrosis is inhibited. Proper increase of uPA activity, inhibition of early activation of TGFβ1 and inhibition of PAI-1 overexpression in the late stage of cirrhosis may be helpful to inhibit the activation of HSC, increase the extracellular matrix degradation, and thus delay the occurrence and development of cirrhosis.