Objective: To study the effect of Qigui Yishen formula (QGYS) on delaying the renal fibrosis by regulating the expression of cell signaling pathway TGF-β/Smad/ILK in unilateral ureteral obstruction (UUO) nephropathy models. Method: The 32 Kunming mice were randomly divided into normal group

model group

benazepril group

and QGYS group

n=8 in each group. All the mice except those in normal group were used to prepare UUO nephropathy models. Corresponding drugs were used in various groups then. Renal tissues were taken after sacrificing on day 10 and were used for HE staining to observe the pathological changes of renal tissues in mice; immunohistochemistry was used to observe transforming growth factor-1 (TGF-β1) of renal tissues

cell signal transduction molecules-2 (Smad2)

type I collagen (Col-I) and integrin linked kinase (ILK) protein expressions; RT-PCR and Western blot were used to observe the mRNA and protein expression levels of TGF-β1

Col-I and ILK. Result: As compared with the normal group

immunohistochemistry results showed that the protein expression levels of TGF-β1

Smad2

Col-I and ILK were significantly increased in renal tissues of model group mice; RT-PCR and Western blot results showed that the mRNA and protein expression levels of TGF-β1

Col-I and ILK were significantly increased in renal tissues of model group mice (P<0.05)

with more obvious renal fibrosis. As compared with the model group

renal fibrosis was relieved in benazepril group

and QGYS group; protein expression levels of TGF-β1

Smad2

Col-I and ILK were significantly reduced (P<0.05)

and the effect in QGYS group was more obvious in that of benazepril group (P<0.05). Conclusion: QGYS could decrease the level of renal fibrosis in UUO nephropathy models

and the action mechanism may be associated with regulating the expression of the cell signaling pathway of TGF-β/Smad/ILK.