Aim:Irbesartan,a new antagonist of the type Ⅰ angiotensin Ⅱ receptor,has beenproven to be renal protective in both diabetic and non-diabetic nephropathy,butits exact mechanism is still uncertain.Here we investigated the influence ofirbesartan on the expression of the integrin-linked kinase (ILK) and its relation-ship with epithelial-mesenchymal transition (EMT) in mice with unilateral ureteralobstruction (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 weightper day by gavage.The experimental animals in the control group received thesame 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 atmRNA and protein levels were significantly increased in the UUO group 1 d afterthe surgery,which was significantly decreased by treatment with irbesartan (P<0.01,respectively).The expression of α-smooth muscle actin (α-SMA) was sig-nificantly increased,while E-cadherin was decreased in mice with UUO at d 3 afterthe surgery.Treatment with irbesartan significantly abrogated such effects (P<0.01).The immunohistochemistry analysis indicated that the protein expressionof the ILK was positively correlated with α-SMA,but negatively with E-cadherin.Conclusion:These results suggested that irbesartan attenuated renaltubulointerstitial fibrosis in UUO mice,which may be related to the inhibition ofILK expression,subsequently preventing the tubular EMT. Aim: Irbesartan, a new antagonist of the type I angiotensin II receptor, has beenproven to be renal protective in both diabetic and non-diabetic nephropathy, butits exact mechanism is still uncertain. Here we investigated the influence of antibodies on the expression of the integrin- linked kinase (ILK) and its relation-ship with epithelial-mesenchymal transition (EMT) in mice with unilateral ureteralobstruction (UUO). Methods: The mice were randomly divided into 3 groups: sham operation n = 40), and UUO with irbesartan treatment (UUO + irbesartan, n = 40) .Irbesartan was given at a dose of 50 mg / kg body weightper day by gavage.The experimental animals in the control group received the 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 atmRNA and protein levels were significantly increased in the UUO group 1 d afterthe surgery, which was significantly decreased by treatment with irbesar The expression of α-smooth muscle actin (α-SMA) was sig-nificantly increased, while E-cadherin was decreased in mice with UUO at d 3 afterthe 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. ConCL: These results suggested that irbesartan attenuated renal tubulointerstitial fibrosis in UUO mice, which may be related to the inhibition ofILK expression, successively preventing the tubular EMT.