Aim:Irbesartan,a new antagonist of the type 1 angiotensin Ⅱ receptor,has been proven to be renal protective in both diabetic and non-diabetic nephropathy,but its exact mechanism is still uncertain. Here we investigated the influence of irbesartan on the expression of the integrin-linked kinase (ILK) and its relationship with epithelial-mesenchymal transition (EMT) in mice with unilateral ureteral obstruction (UUO). Methods:The mice were randomly divided into 3 groups:sham operation (C,n=20),UUO (n=40),and UUO with irbesartan treatment (UUO+irbesartan,n=40). Irbesartan was given at a dose of 50 mg/kg body weight per day by gavage. The experimental animals in the control group received the same volume of vehicle (0.9% saline solution). The animals were sacrificed at d 1,3,7,and 14,respectively,after the surgery. Results:The expression of the ILK at mRNA and protein levels were significantly increased in the UUO group 1 d after the surgery,which was significantly decreased by treatment with irbesartan (P＜0.01,respectively). The expression of α-smooth muscle actin (α-SMA) was significantly increased,while E-cadherin was decreased in mice with UUO at d 3 after the surgery. Treatment with irbesartan significantly abrogated such effects (P＜0.01). The immunohistochemistry analysis indicated that the protein expression of the ILK was positively correlated with α-SMA,but negatively with E-cadherin.Conclusion:These results suggested that irbesartan attenuated renal tubulointerstitial fibrosis in UUO mice,which may be related to the inhibition of ILK expression,subsequently preventing the tubular EMT.