中国寄生虫学与寄生虫病杂志 ›› 2004, Vol. 22 ›› Issue (3): 7-156.

• 论著 • 上一篇    下一篇

Smads在日本血吸虫病小鼠肝纤维化形成过程中的表达

张彬彬,焦杨文,蔡卫民,陶君,郑敏,董凤芹,刘荣华
  

  1. 浙江大学医学院附属第一医院传染病研究所,杭州 310003
  • 收稿日期:1900-01-01 修回日期:1900-01-01 出版日期:2004-06-30 发布日期:2004-06-30

Studies on Smads at Transcription Level in Liver Fibrosis of Mice with Schistosomiasis japonica

ZHANG Bin-bin,JIAO Yang-wen,CAI Wei-min,TAO Jun,ZHENG Min,DONG Feng-qin,LIU Rong-hua
  

  1. Institute of Infectious Diseases,First Affiliated Hospital of School of Medicine,Zhejiang University,Hangzhou,31003,China
  • Received:1900-01-01 Revised:1900-01-01 Online:2004-06-30 Published:2004-06-30

摘要:   目的 从转录水平研究参与转化生长因子β1(transforminggrowthfactor beta 1,TGF β1)信号传导的Smads分子在日本血吸虫病小鼠肝纤维化形成过程中的表达。 方法 以日本血吸虫尾蚴感染BALB/c小鼠形成肝纤维化动物模型,分别于感染后第 8、12、16和24周取小鼠肝组织 ,作病理学检测,观察肝纤维化程度,采用逆转录聚合酶链反应(RT PCR)的方法检测模型组和正常组小鼠肝组织中Smad2、Smad3、Smad4和Smad7的mRNA水平。 结果 Smad 2mRNA水平在感染12周后表达下降(P<0.05),16周后恢复正常,2 4周后再次下降(P<0.05)。Smad 3mRNA水平在感染后 16周开始明显升高 ,达正常水平的2倍(P<0.05)。Smad4和Smad7的mRNA水平在肝纤维化形成过程中与正常组比较无明显差异。 结论 Smad3促进肝纤维化形成。Smad2对肝纤维化形成具有双效性 ,即感染初期属于促进因子 ,感染后期属于抑制因子。

关键词: 日本血吸虫病, 肝纤维化, 转化生长因子β1, Smad, 逆转录聚合酶链反应

Abstract:  Objective To study Smads involved in TGF-β signal transduction at the transcription level during the development of liver fibrosis in BALB/c mice infected by Schistosoma japonicum. Methods BALB/c mice infected with cercariae of S. japonicum were used as liver fibrosis models. Liver specimens were harvested at 8,12,16 and 24 weeks after infection and normal control were sacrificed at the 24th week. A part of the liver specimens were preserved for pathologic examination and the other part was frozen for the detection of mRNA level of Smad 2,Smad 3,Smad 4 and Smad 7. Results The level of Smad 3 mRNA was significantly higher than that of control at the later stage, while the mRNA level of Smad 2 decreased at 12 and at 24 weeks,respectively. No significant difference in the mRNA level of Smad 4 and Smad 7 was observed between the infection group and the control. Conclusion Smad 3 may induce the development of liver fibrosis in mice infected by S. japonicum while Smad 2 may induce the development of liver fibrosis at early stage and inhibit it at later stage.

Key words: Schistosomiasis japonica, Liver fibrosis, Transforming growth factor-β 1, Smad, RT-PCR