To investigate the dynamic changes of signal transducer and activator of transcription 3(STAT3)mRNA expression in the process of liver fibrosis formation and study the molecular action mechanism of Benazepril in treating the liver fibrosis model, and to provide an experimental evidence for the new drug treating of liver fibrosis.

SD rats were randomly divided into three groups using random number table method: control group(n=6), model group(n=26)and Benazepril intervention group(n=8). Both hematoxylin-eosin(HE)staining and Masson staining were performed to evaluate the degree of liver damage and liver fibrosis.The expression change of STAT3 mRNA was determined by reverse transcription polymerase chain reaction(RT-PCR).

STAT3 mRNA expression was gradually increased in the process of liver inflammation and fibrosis, and it reached the peak at 6 weeks(221.459±51.362), while declined at the 8 weeks(120.939±24.764), obviously higher than that in control group(51.160±16.427, P<0.05). When intervened with Benazepril, STAT3 mRNA expression was significantly decreased compared with model group(75.031±9.203 vs.120.939±24.764, P<0.05).

STAT3 is possibly an indispensable key member in the process of liver fibrosis induced by liver damage and chronic hepatitis.Benazepril may further inhibit hepatic stellate cell activation via inhibiting STAT3 mRNA and therefore plays an efficient role against liver fibrosis.