Abstract: Objective To investigate the expression and the possible mechanism of microRNA-21(miR-21) and Ski-related novel protein N(SnoN) in the renal fibrosis diabetic process. Methods The diabetic rats were established by tail-vein injection of Streptozotocin,and the other group were normal control(NC) group. After 10 weeks, the rats were sacrificed to detect relative biochemical parameters and renal index, and to observe the changes of pathomorphology by HE staining as well. Meanwhile, immunohistochemistry and Western blot were employed to detect the protein expression of E-cadherin,α-smooth muscle actin(α-SMA), fibronectin(FN), collagen-I(Col-I), collagen-Ш(Col-Ш), transforming growth factor-β1(TGF-β1), Smad3, p-Smad3(Ser423/425) and SnoN in the renal tissue. In addition, the expression of SonN mRNA and miR-21 were detected by qPCR. Results In DM group,the expressions of Col-I、Col-Ш and FN in renal interstitium were increased(P<0.05)，TGF-β1 increased(P<0.05) ，while E-cadherin decreased(P<0.05). Compared with NC group, the expression of α-SMA、p-Smad3(Ser423/425)protein increased in DM group(P<0.05)，while the protein level of SnoN decreased but the level of SnoN mRNA increased(P<0.05). Moreover, the level of miR-21 markedly increased in DM group(P<0.05). Conclusion TGF-β1 may up-regulate the expression of miR-21 but restrain the translational expression of SnoN, aggravating fibrosis.

Key words: Key words: diabetic nephropathy, Ski-related novel protein N(SnoN) protein, p-Smad3(Ser423/425) protein, microRNA-21 (miR-21).