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纤溶酶原激活物抑制剂-1在大鼠肝纤维化组织中的表达及其与Ⅰ、Ⅲ型胶原的相关性分析 被引量:6

Expression of plasminogen activator inhibitor-1 in hepatic fibrosis and correlation with collagen Ⅰ、Ⅲ in rats
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摘要 目的探讨纤溶酶原激活物抑制剂-1(plasminogen activator inhibitor-1,PAI-1)与肝纤维化发生的关系。方法采用皮下注射四氯化碳(CCl4)的方法制备大鼠肝纤维化模型,根据注射时间的不同,获取组织标本,行苏木精-伊红和VG染色,明确纤维化分期后,利用免疫组织化学及逆转录聚合酶链反应方法,观察PAI-1在肝纤维化进程中的表达变化情况及其与Ⅰ、Ⅲ型胶原的相关性。结果PAI-1在正常大鼠肝脏中,仅在汇管区细胞浆有少量表达,而随着纤维化的进展,其表达量进行性增加;在纤维化肝脏,PAI-1主要分布于细胞浆;PAI-1与Ⅰ、Ⅲ型胶原呈直线相关。结论PAI-1在肝纤维化进程中持续上调,可能参与胶原的表达调控,在肝纤维化的发生中起重要作用。 Objective To investigate the relationship between expression of plasminogen activator inhibitor-1 (PAI-1) and development of hepatic fibrosis. Methods Rat hepatic fibrosis was induced by subcutaneous injection of carbon tetrachloride( CCl4 ) and the rat livers were obtained for study after 2 and 6 weeks injection. The different stages of fibrosis were confirmed with H-E and VG staining, and the expression of PAI-1 at transcription and translagtion level was detected by reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry. Expression and correlation of PAI-1 with collagen in the development of rat hepatic fibrosis were analyzed. Results There was only weak expression of PAI-1 in normal liver, and the expression increased with the development of fibrosis, which was mainly located within. The expression of PAI-1 was well correlated with the amout collagen type Ⅰ and Ⅲ during the development of hepatic fibrosis. Conclusion PAI-1 is up-regulated in fibrotic liver, which might be invoIved in the production of collagen, and play an important role in the pathogenesis of hepatic fibrosis.
出处 《肝脏》 2006年第1期18-20,共3页 Chinese Hepatology
基金 2005上海市青年科技启明星跟踪计划(05QMH1406)
关键词 纤溶酶原激活物抑制剂-1 肝纤维化 Ⅰ型胶原 Ⅲ型胶原 Plasminogen activator inhibitor-1 Hepatic fibrosis Collagen type Ⅰ Collagen type Ⅲ
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参考文献2

  • 1Louis H,LeMoine A,Quertinmont E,etal.Repeated concanavalin A challenge in mice induces an interleukin 10-producing phenotypeand liver fibrosis.Hepatology,2000,31:381-390.
  • 2Kovalovich K,DeAngelis RA,Li W,et al.Increased toxin induced liver injury and fibrosisin interleukin-6-deficient mice.Hepatology,2000,31:149-159.

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