A Study On TGF-β/Smads Path Mediating The Treatment Effects Of AKF-PD On Rat Chronic Hepatic Injury Induced By DEN

Objective:To investigate the possible mechanism of AKF-PD on chronic hepatic injury in rat and provide theory basis for its further optimization of the process and clinic application.Method:1. We established the model of rat chronic liver injuries induced by DEN and adopted AKF-PD to treat. Rats were randomly divided into3groups:control group, DEN group and AKF-PD treatment group. Observing the general state of rats’health, detecting serum ALT and AST level and observing the pathology change by HE, Masson staining in each group. Determining the mRNA expression of a-SMA, TGF-β1, Smad3, Smad7and the protein expression of Smad3, Smad7in hepatic tissue and hepatic cell to evaluate the prophylactic treatment mechanism of AKF-PD on rat chronic liver injuries.Results:We successfully established the model of rat chronic liver injuries induced by DEN. Rats’serum ALT level was significantly increased in the ninth week in DEN group and rats’serum ALT, AST level was significantly heightened in the sixteenth week in DEN and AKF-PD treatment group. DEN induced hepatocyte steatosis and hepatic inflammation in rats in DEN group. The mRNA and protein expression of a-SMA, TGF-β1, Smad3were significantly increased but the mRNA and protein expression of Smad7was significantly decreased in hepatic tissue in DEN group. The mRNA and protein expression of a-SMA, TGF-β1, Smad3, Smad7were opposite in hepatic tissue in AKF-PD treatment group to group. Before the ninth week, the mRNA expression of a-SMA, TGF-β1was significantly increased in hepatic cell in DEN group. After the ninth week, the mRNA expression of a-SMA, TGF-β1, Smad3was significantly decreased in hepatic cell in AKF-PD treatment group but the mRNA expression of Smad7was significantly increased. The protein expression of Smad3was significantly increased but the protein expression of Smad7was significantly decreased in hepatic cell in DEN group. AKF-PD had no effect for the protein expression of Smad3, Smad7in hepatic cell.Conclusion:1. We successfully established the model of rat chronic liver injuries induced by DEN.2. AKF-PD could inhibit the activation of HSC and lessen chronic liver injuries. It decreased the mRNA and protein expression of α-SMA, TGF-β1, Smad3and increased the mRNA and protein expression of Smad7in hepatic tissue.3. AKF-PD could inhibit the mRNA expression of α-SMA, TGF-β1, Smad3and increased the mRNA expression of Smad7in hepatic cell but had no effect for the protein expression of Smad3, Smad7in hepatic cell.