Effect Of TGF-β1siRNA On Smad Proteins In Hepatic Fibrosis Rats

Objective: To observe changes in Smad2,3,4, and7of thetransforming growth factor beta1(TGF-β1)/Smad signaling pathways incarbon tetrachloride (CCL4)-induced hepatic fibrosis in rats treated withTGF-β1short interference RNA (siRNA).Methods: Liver tissues were collected from rats with liver fibrosisafter receiving TGF-β1siRNA treatment. We divided the liver tissuesamples into5groups: normal group, model group, TGF-β1siRNAnegative control group, TGF-β1siRNA0.125mg/kg group and TGF-β1siRNA0.250mg/kg group. We detected the protein expression of Smad2,3,4, and7by immunohistochemistry and western blot and the mRNAexpression of Smad2,3,4, and7using real-time polymerase chain reaction(RT-PCR).Result: When comparing the protein and mRNA expression of Smad2,3and4, the TGF-β1siRNA0.250mg/kg and TGF-β1siRNA0.125mg/kggroups were lower than the model and the TGF-β1siRNA negative controlgroups (P<0.05). The protein and mRNA expression levels of Smad2,3,and4in the TGF-β1siRNA0.250mg/kg group were lower than in the0.125mg/kg group (P<0.05). Comparing the TGF-β1siRNA0.250mg/kg and siRNA0.125mg/kg groups to the model group and the TGF-β1siRNAnegative control group showed significantly increased levels of proteinexpression and mRNA expression of Smad7(P<0.05). In addition, theseexpression levels of smad7were higher in the TGF-β1siRNA0.250mg/kggroup than in the0.125mg/kg group (P<0.05).Conclusions: After TGF-β1siRNA interference of the expression ofTGF-β1in rats, Smad2,3, and4expression levels were significantlyreduced, but Smad7expression was increased.This regulative efficacycould be involved in the improvement of the hepatic fibrosis in rats.