Effects Of Benazepril On STAT3 MRNA In Rats With Hepatic Fibrosis

Objective:To investigate the dynamic changes of angiotensin II(AngII)and signal transduction transcription factor(STAT3 mRNA)in carbon monoxide(CCL4)liver fibrosis rats and study the molecular action mechanism of Beinapuli in treating the liver fibrosis model.The Correlation of STAT3 m RNA and RAS system may provide a new clinical ideas in the treatment of liver fibrosis.Methods:SD rats were randomly divided into three groups: control group(n=6),model group(n=26)and Benazepril treatment group(n=8).The model group and the treatment group of rats were subcutaneously injected with 40% CCL4,2 times a week,for the first time,the amount of 5ml/kg,followed by 2.0ml/kg.The amount of CCL4 was adjusted according to the weight.The normal control group of rats were given the same dose of edible oil subcutaneously.The rats in the treatment group were given 10mg/kg of Benazepril irrigation and the other two groups were given the same dose of normal saline until the end of the experiment.6 rats were killed on the end of 2weeks,4weeks,6weeks and 8weeks in the model group.6 rats were killed at the end of 8 weeks in the control group and treatement group.Histopathological study of liver tissue was done with hematoxylin-eosin(HE)and masson trichrome staining.The concentration of AngII was determined by enzyme linked immunosorbent assay.Real-time quantitative PCR was used to detect STAT3 m RNA.Results:(1)HE and Masson staining: Compared with the control group,with the continuous stimulation of CCL4,the degree of rats liver lipid steatosis,inflammatory injury,necrosis and fibrosis gradually increased(P<0.05)in the model group;compared with the model group,Benazepril significantly reduced the damage,necrosis and fibrosis of hepatocytes(P<0.05).(2)ELISA results showed that the concentration of AngII of liver tissue of the model group were higher than the control group(P<0.05).(3)The results of PCR showed that the expression of STAT3 mRNA in the liver tissue of the model group was significantly higher than that in the normal group(P<0.05).The expression of STAT3 mRNA in the liver tissue of the treatment group was significantly lower than that in the model group(P<0.05).(4)The level of AngII was positively correlated with the expression of STAT3 mRNA.Conclusion:(1)In the process of hepatic fibrosis in rats,STAT3 and AngII were gradually increased.(2)STAT3 and AngII were positively correlated.(3)Benazepril,the angiotensin-converting enzyme inhibitor,decreased the expression of STAT3 m RNA,which suggest that inhibition of STAT3 protein-related pathways may be one of its mechanisms of anti-fibrosis.