Smurf1和Smurf2在人肝纤维化过程中的表达及意义

发布时间：2018-03-17 20:44

  本文选题：肝纤维化　切入点：Smurf　出处：《广西医科大学》2014年硕士论文　论文类型：学位论文

【摘要】：目的:观察Smurf1、Smurf2、Smad3和Smad7蛋白在人肝纤维化组织中的表达，探讨四者的相互关系及介导的信号传导在肝纤维化发生中的作用机制。 方法:采用免疫组织化学法测定9例正常肝组织和38例慢性HBV感染者肝组织中Smurf1、Smurf2、Smad3和Smad7的表达情况。 结果:Smurf1、Smurf2、Smad3和Smad7在肝内实质细胞及非实质细胞均可见广泛表达。与正常肝相比，肝纤维化组Smad3表达显著增加（Z=-3.110，P=0.002），Smurf2表达亦明显增加（Z=-2.716，P=0.007），Smad7表达显著降低（Z=-2.899，P=0.004）；而Smurf1表达无显著变化（Z=-1.399，P=0.162），差异无统计学意义。Smad3与纤维化程度呈显著正相关（r=0.627，P=0.000）；Smad7与纤维化程度呈显著负相关（r=-0.488，P=0.000）；Smurf1与肝纤维化无显著相关性（r=-0.064，P=0.670），Smurf2与纤维化程度呈显著正相关（r=0.652，P=0.000）。Smurf2与Smad3呈显著正相关（r=0.523，，P=0.000），与Smad7呈显著负相关（r=-0.447，P=0.002）；Smurf1与Smurf2、Smad3、Smad7无相关性（r=-0.008、r=-0.053、r=0.219，P＞0.05）；Smad3与Smad7呈负直线相关（r=-0.389，P=0.007）。 结论：Smad3信号增强及Smad7信号缺失可能导致肝纤维化发展,Smurf1在肝纤维化的发展过程中能发挥的调控作用有限，Smurf2在肝纤维化进展中发挥双向调节作用,但对TGF-β1/Smad信号通路的促进作用大于其抑制作用。
[Abstract]:Aim: to investigate the expression of Smurf1, Smurf2, Smad3 and Smad7 proteins in human liver fibrosis, and to explore the relationship between the four proteins and the mechanism of signal transduction in the pathogenesis of liver fibrosis. Methods: the expression of Smurf1 Smurf2 Smad3 and Smad7 in 9 cases of normal liver tissue and 38 cases of chronic HBV infection were detected by immunohistochemical method. Results both Smurf2 Smad3 and Smad7 were widely expressed in parenchymal cells and non-parenchymal cells. In liver fibrosis group, the expression of Smad3 increased significantly, and the expression of Smurf2 increased significantly in the liver fibrosis group. The expression of Smad7 decreased significantly, while the expression of Smurf1 did not change significantly. There was no significant difference between Smad3 and the degree of fibrosis. There was a significant negative correlation between Smad7 and the degree of fibrosis. There was no significant correlation between Smurf1 and liver fibrosis. There was a significant positive correlation between Smurf2 and the degree of fibrosis. There was a significant positive correlation between Smurf2 and Smad3. There was a significant negative correlation between Smurf1 and Smurf1 and Smurf1, Smurf1 and Smurf2Smad3Smad7. There was no significant correlation between Smurf1 and Smurf2 and Smurf2Smad3Smad7. There was no significant correlation between Smurf1 and Smurf2 and Smurf2Smad3Smad7. There was no significant positive correlation between Smurf1 and Smurf2 and the degree of fibrosis. There was a significant positive correlation between Smurf2 and Smad3. There was no significant correlation between Smurf1 and Smurf1 and Smurf2Smad3Smad7. There was no significant positive correlation between Smurf1 and Smurf2 and Smurf2 were positively correlated with Smad3, and there was no significant correlation between Smurf1 and Smurf1 with Smurf2Smad3Smad7. Conclusion the enhancement of Smad3 signal and the absence of Smad7 signal may lead to the development of hepatic fibrosis. Smurf1 may play a limited regulatory role in the development of liver fibrosis. Smurf2 may play a bidirectional regulatory role in the progression of liver fibrosis. However, the promotion of TGF- 尾 1 / Smad signaling pathway was greater than its inhibitory effect.
【学位授予单位】：广西医科大学
【学位级别】：硕士
【学位授予年份】：2014
【分类号】：R575

【参考文献】

相关期刊论文 前2条

1 张国,张法灿,王天才,梁扩寰;活血软坚方对肝星状细胞Smad信号的影响及意义[J];中华肝脏病杂志;2004年04期

2 陈伟 ,付小兵 ,盛志勇;Review of current progress in the structure and function of Smad proteins[J];Chinese Medical Journal;2002年03期

本文编号：1626402