Abstract
Liver fibrosis is a pathological process of chronic liver diseases. In particular, epithelial‑mesenchymal transition (EMT) is a major source of myofibroblast structure in liver fibrosis. The present study investigated the effects of recombinant truncated transforming growth factor‑ß receptor II (rtTGFβRII) on EMT and liver fibrosis in a carbon tetrachloride (CCl4)‑induced rat model. A total of 24 rats were randomly separated into three groups: Normal control (NC), model (CCl4) and treatment (CCl4 + rtTGFβRII) groups. Histological methods, including hematoxylin and eosin, Masson's trichrome and Sirius red staining were conducted. The activities of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured using an automatic biochemical analyzer. The mRNA expression levels of fibroblast specific protein‑1 (FSP‑1), α‑smooth muscle actin (α‑SMA), fibronectin, collagen I, vimentin and E‑cadherin were detected using reverse transcription‑quantitative polymerase chain reaction analysis. The protein levels of fibronectin, collagen I, E‑cadherin, Smad2/3 and phosphorylated (p)‑Smad2/3 were detected using western blot analysis. The expression of α‑SMA, fibronectin, vimentin and E‑cadherin in the liver tissue was detected using immunofluorescence staining. The results demonstrated that invivo, rtTGFβRII significantly reduced the degree of liver injury, serum ALT and AST activities and liver fibrosis. These factors were associated with reduced expression of FSP‑1, α‑SMA, fibronectin, collagen I, vimentin and p‑Smad2/3, and increased expression of E‑cadherin. The results of the present study suggest that rtTGFβRII may inhibit EMT processes in CCl4‑induced liver fibrosis in rats and alter the expression of epithelial and myofibroblast markers. Therefore, rtTGFβRII may be considered a possible treatment for preventing liver fibrosis via EMT processes.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
