Abstract: Objective To investigate the effect of resveratrol on renal fibrosis and kidney damage induced by unilateral ureteral obstruction and its related mechanism. Methods  Sprague-dawley( SD) rats and NRK-49F fibroblasts were used as experimental subjects for in vivo study and in vitrovalidation. In vivo, TIF rat model was establish by surgery to induce the unilateral ureteral obstruction in SD rats, and the rats were then randomly divided into 4 groups: sham operation + blankgroup, sham operation + resveratrol group, model + blank group and model + resveratrol group, 12rats in each group. In vitro: NRK-49F cells were treated with recombinant TGF-β1 (5 ng / mL) orresveratrol (10 and 100 μmol / L) and randomly divided into 4 groups: control group, TGF-β1 group, TGF-β1 + resveratrol low-dose group and TGF-β + resveratrol high-dose group. Masson’ s staining was used to detect total collagen deposition in the kidney. Immunohistochemical staining was used to detect the expression of E-cadherin, GFAP and Ki67 in the tissues. Immunofluorescence staining was used to detect the expression of Ki67 in cells. Western blotting was used to detect the expression level of Vimentin, N-cadherin, Racl, c-Myc, Bcl-2, Cyclin D1, α-SMA, type I collagen and type Ⅲ collagen, E-cadherin. Results Resveratrol could inhibit the excessive depositionof total collagen in kidneys of UUO rats, down-regulate α-SMA-positive myofibroblasts, reduce the expression of vimentin, type I and type Ⅲ collagen, and inhibit the up-regulation of Rac1, GFAP and down-regulation of N-cadherin. Resveratrol could significantly reduce the ratio of Ki67-positive cells in UUO rats and inhibit the expression level of c-Myc, Bcl-2 and cyclin D1. Resveratrol inhibited the activation of proliferation-related pathway Wnt / β-catenin. The in vitro experimentsshowedthat resveratrol treatment could reduce the proliferation of fibroblasts and TECs, thereby inhibiting

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