bFGF及TGF-β_1在实验性肝硬化中的免疫组化研究

Immunohistochemical expression of bFGF and TGF-β_1 in experimental cirrohosis rats

目的 观察碱性成纤维细胞生长因子 (BasicFibroblastGrowthFactor ,bFGF)及转化生长因子 β1 (TransformingGrowthFac tor Beta1,TGF β1 )在实验性肝硬化大鼠不同时期的免疫组化表达和定位情况 ,探讨二者在肝纤维化发生过程的作用及两者相关性。方法 用硫代乙酰胺 (Thioacetamide ,TAA)诱导肝硬化动物模型 ,采用免疫组化、计算机图像分析等技术 ,动态观察bFGF及TGF β1在正常对照组及肝硬化模型组不同时期的表达和定位特点 ,各组间进行统计学比较。结果 bFGF在实验性肝硬化不同发展阶段 ,其表达逐渐增高 ,差异有显著性 (P <0 0 5 )或高度显著性 (P <0 0 1) ,TGF β1 在实验性肝硬化不同发展时期 ,其表达亦逐渐增高差异有显著性 (P <0 0 5 )或高度显著性 (P <0 0 1)。实验组中bFGF及TGF β1 之间的表达可见高度显著性正相关 (r =0 98,P <0 0 0 1)。结论 bFGF在实验性肝硬化发生发展过程中 ,起着重要促进作用 ,TGF β1 同样在实验性肝纤维化发生发展中起着关键作用 ,bFGF及TGF β1 可能存在协同致肝纤维化作用 ,可作为评价肝纤维化严重程度的重要指标之一 ,同时也为今后以bFGF及TGF β1

Objective To study the immunolocation and expression of transforming growth factor-beta1(TGF-β_1) and the basic fibroblast growth factor (bFGF) in different stage on experimental rat hepatic cirrohosis and to discuss the possible effects and correlation in the development of liver fibrosis.Methods Liver cirrohosis model rats were setup by thioacetamide(TAA). In all the tested animals, their liver tissues were obtained for pathological observation and immunohistochemistry staining. The expression degree of bFGF and TGF-β_1 and the changes of morphology in liver were measured by image analysis system.Results Cirrohosis models were successfully constructed. The expression of bFGF and TGF-β_1 were gradually increased in the different pocesses of experimental hepatic cirrohosis rats, respectively(P<0.01or P<0.05). There was obvious positive correlation between the expression of bFGF and the expression of TGF-β_1(r=0.98, P<0.001).Conclusions bFGF may play an important role in the development of hepatic fibrosis. In addition, TGF-β_1 also perform a central role in the processes of experimental hepatic fibrosis. bFGF and TGF-β_1 play a reciprocal promoting role to lead to the liver fibrosis. They can be regarded as one of the important markers to predict the severe degree and consequence of liver fibrosis. Our results provide theory foundation for us to target liver fibrosis through bFGF and TGF-β_1.