ObjectiveTo study the effect of valsartan, an angiotensinⅡtypeⅠreceptor antagonist（AT1RA）, on renal interstitium fibrosis（RIF）in rats with unilateral ureteral obstruction （UUO）, and to discuss the possible mechanisms. MethodsThirty-five Sprague-Dawley rats were randomly divided into sham-operation, model and valsartan groups.The rat UUO model was established. From the day after operation,the rats in sham-operation and model groups received intragastric valsartan and sodium chloride in tales doses. The serum creatinine（SCr）, blood urea nitrogen（BUN）, angiotensin-Ⅱ(AngⅡ) in blood plasma, N-acetyl-β-D-glucosaminidase（NAG）and 24 h urine β2-microglobulin（β2-MG）were examined 4 weeks after operation. The renal tissues of the obstructed sides were harvested; H-E staining and Masson staining were used to observe the tubulointerstitial lesions; and immunohistochemistry staining was used for semiquantitative analysis of alpha-smooth muscle actin（α-SMA）, fibronectin（FN）, plasminogen activator inhibitor-1（PAI-1）, transforming growth factor-beta 1（TGF-β1）, and hepatocyte growth factor（HGF）.ResultsCompared with those in the sham-operation group, SCr, BUN, AngⅡ, NAG and β2-MG levels,and the expression of α-SMA,FN,PAI-1,and TGF-β1 in model group were significantly higher（P<0.01）. The levels of SCr,BUN,NAG and β2-MG were comparable between valsartan group and the model group（P>0.05）. The expression levels of α-SMA,FN,PAI-1,and TGF-β1 in valsartan group were significantly lower than and the expression of HGF was significantly higher than those in the model group（P<0.01）. ConclusionValsartan does not improve the tubular and glomerular functions, but it can inhibit production of Ang-II. Valsartan may inhibit renal interstitial fibrosis by inhibiting renal tubule epithelial mesenchymal transdifferentiation and reducing extracellular matrix deposition through blocking up AngⅡ, inhibiting overexpression of α-SMA,FN,PAI-1, and TGF-β1, and inducing the HGF expression.