Effect Of Truncated TGF-β Type II Receptor On Epithelial-mesenchymal Transition In Rats With Hepatic Fibrosis

Objective:Liver fibrosis is a mutual pathological process of chronic liver diseases.In particular,epithelial-mesenchymal transition（EMT）is a major source of myofibroblast structure in liver fibrosis.This research investigated the effects of recombinant truncated transforming growth factor-beta receptor II（rtTGFβRII）on liver fibrosis and EMT in a carbon tetrachloride（CCl₄）-induced rat model.Methods:Twenty-four rats were separated into three groups randomly:normal control（NC）,model（CCl₄）and treatment（CCl4+rtTGFβRII）.We used automatic biochemical analyzer to measure the activities of serum alanine aminotransferase（ALT）and aspartate aminotransferase（AST）.Histological methods were assessed using hematoxylin and eosin（H&E）,Masson’s trichrome（MTS）and Sirius red staining.The mRNA levels of fibroblast specific protein-1（FSP-1）,α-smooth muscle actin（α-SMA）,Fibronectin,type I collagen（Collagen I）,Vimentin and E-cadherin were detected using real-time PCR（RT-PCR）analysis.The expression ofα-SMA,Fibronectin,Vimentin and E-cadherin in the liver tissue was detected using immunofluoresence staining.The protein levels of Fibronectin,Collagen I,E-cadherin,Smad2/3 and p-Smad2/3 were detected using western blot analysis.Results:The results demonstrate that in vivo,rtTGFβRII significantly reduced the activities of serum ALT and AST（P<0.05）,the degree of liver injury,and liver fibrosis,which was associated with reduced（P<0.05）expression of FSP-1,α-SMA,Fibronectin,Collagen I,vimentin and p-Smad2/3 while increased（P<0.05）expression of E-cadherin.Conclusions:The results in this research suggests that rtTGFβRII inhibits EMT processes in CCl₄-induced liver fibrosis in rat,with changed expression of epithelial and myofibroblast markers.In addition,rtTGFβRII is a possible treatment for preventing liver fibrosis via EMT processes.