TGFβ_1-Smad3-ILK信号转导通路与大鼠肝纤维化的相关性研究

Correlational study between the TGFβ_1-Smad3-ILK signal transduction pathway and hepatic fibrosis of rat

目的研究TGFβ1-Smad3-ILK信号转导通路与大鼠肝纤维化的关系。方法建立40%CCl4诱导的大鼠肝纤维化模型。60只SD大鼠随机分为5组:正常对照组、模型2周组、模型4周组、模型6周组、模型8周组。对模型2、4、6、8周组及对照组大鼠行HE染色、网状纤维染色、免疫组织化学反应,观察肝组织病理变化、纤维增生及ILK和TGFβ1-Smad3的表达情况。结果免疫组织化学染色显示,ILK和TGFβ1-Smad3在正常的肝组织中几乎没有表达。在注射CCl4后,大鼠肝脏组织中ILK和TGFβ1-Smad3较正常对照组表达明显增强,模型2、4、6、8周组中ILK和TGFβ1-Smad3的表达程度呈明显递增趋势,表明大鼠肝组织纤维化与ILK和TGFβ1-Smad3的表达有关。结论 ILK和TGFβ1-Smad3的表达可能与大鼠肝纤维化有联系,如能继续深入研究TGFβ1-Smad3-ILK信号转导通路在肝纤维化中的发生机制,或许可为肝纤维化的防治提供新的理论依据。

Objective To study the relationship between TGFβ1-Smad3-ILK signal transduction pathway and hepatic fibrosis of rats. Methods The 40% CC14 induced hepatic fibrosis SD rat model was established and 60 rats were randomly divided into five groups：normal control group,model 2 weeks groups,model 4 weeks group,model 6 weeks group and model 8 weeks group respectively.The liver tissue of all groups of rats were given HE staining,reticular fiber stain- ing,immunohistoehemical reaction.The pathological changes,fibroplasia,ILK and TGFβ1-Smad3 expression were ob- served. Results Immunohistochemical staining shows no expression of ILK and TGFβ1-Smad3 in normal liver tissue, while after 4 weeks of CC14 injection,the expression obviously increased,in addition,a progressive increasement was observed after 2,4,6,8 weeks of injection,which indicates that there was a relationship between TGFβ1-Smad3 expression and hepatic fibrosis of rats. Conclusion ILK and TGFβ1-Smad3 expression maybe related to the rat hepatic fibrosis,if the occurrence mechanism of TGFβ1-Smad3-ILK signal transduction pathway being sthdied deeply,there will be a new theory basis for hepatic fibrosis prevention and treatment.