Objective To study the possible mechanism of Yishen Huayu Formula（ formula to supplement the kidney and transform stasis） for renal interstitial fibrosis. Methods Totally 108 Sprague Dawley rats were randomized into the sham operation group

model group

valsartan group and Yishen Huayu Formula high-dose

middle-dose and low-dose groups

with 18 in each. The models of renal interstitial fibrosis were established by unilateral ureteral obstruction in all groups except the sham operation group. On the 2nd day after modeling

Yishen Huayu Formula highdose

middle-dose and low-dose groups were gavaged with 32 g /kg·d

16 g /kg·d and 8 g /kg·d of Yishen Huayu Formula concentrated solution respectively

valsartan group was gavaged with 13. 3 mg /kg·d of valsartan solution and sham operation group and model group were gavaged with 20 ml / kg·d of normal saline for 28 days. The pathological changes in kidney tissue were observed on the 7th

14 th

and 28 th day after modeling. The renal interstitial fibrosis area was calculated. The expressions of transforming growth factor-β1（ TGF-β1） and Smad7 signaling proteins were detected. Results There were renal interstitial infiltration of inflammatory cells

spindle nucleated cell proliferation and focal renal interstitial fibrosis in the model group. The pathological manifestations were reduced in all medication groups. The pathological changes in Yishen Huayu Formula high-dose group were the same as in valsartan group.Comparing with the sham operation group

the renal interstitial fibrosis areas and TGF-β1 levels were significantly increased and the Smad7 levels were significantly decreased in other groups（ P < 0. 01）. Comparing with the model group at the same time point

the renal interstitial fibrosis areas and TGF-β1 levels were significantly decreased and the Smad7 levels were significantly increased in all medication groups（ P < 0. 05 or P < 0. 01）

especially in Yishen Huayu Formula high-dose group and valsartan group（ P < 0. 05）. Conclusion Yishen Huayu Formula can reduce renal interstitial fibrosis possibly by inhibiting the expression of TGF-β1 and up-regulating the expression of Smad7.