Recent studies have reported that CTS can alleviate cardiac fibrosis. However, the effects of CTS on kidney fibrosis and EMT are still unknown. This study explored whether CTS could attenuate tubulointerstitial fibrosis as well as EMT, and investigated the potential underlying mechanisms. In this study, an in vivo UUO mouse model and an in vitro TGF-β1 stimulated normal renal tubular kidney epithelial cell model were established. In UUO model, administration of 50 mg kg-1 day-1 CTS markedly decreased the occurrence of kidney injury and the accumulation of fibronectin and collagen-1. In addition, CTS reduced the expression level of α-SMA but retained E-cadherin in obstructed kidneys. In vitro, CTS suppressed the expression of fibronectin, collagen-1 and α-SMA but retained that of E-cadherin. Furthermore, CTS selectively abolished the activation of Smad3 and suppressed the nuclear translocation of Smad2, Smad3 and Smad4. CTS could block the promoter activity of integrin β1 induced by Smad3. Furthermore, CTS inhibited Smad3 binding to integrin β1 promoter sequences. These data suggest that CTS can ameliorate kidney fibrosis and EMT, at least in part, by inhibiting the TGF-β1/Smad3/integrin β1 signaling pathway.