Objective:To investigate the protective effects of salvianolic acid-B (Sal B) on the trans-differentiation of renal tubular epithelial cells and to elucidate the mechanism of Sal B on renal fibrosis. Methods:Human kidney proximal tubular cell line (HK-2) was used as the proximal tubular cell model. Cells were divided into six groups as follows:control group,transforming growth factor-β1 (TGF-β1) (5 ng/ml) group,TGF-β1 (5 ng/ml) plus Sal B (0.1 μmol/L,1 μmol/L,10 μmol/L,and 100 μmol/L) groups. Epithelialto-mesenchymal transition(EMT) was induced with 5 ng/mL of human TGF-β1. The effect of Sal B on cell morphology was observed by phase contrast microscopy,and the expressions of α-smooth muscle actin(α-SMA) and E-cadherin were measured by immunocytochemistry and RT-PCR. Results:Our results revealed that Sal B not only prevented the expression of α-SMA but also prohibited the decrease of the epithelial marker E-cadherin in HK-2 cells in a dose-dependent manner. Simultaneous incubation of Sal B with TGF-β1 could protect the change to the myofibroblast phenotype and restored the epithelial morphology of the HK-2 cells. Conclusion:These observations strongly suggest that Sal B is a potent inhibitor of TGF-β1-induced EMT and may be a promising agent for treating tubulointerstitial fibrosis.