OBJECTIVE: To explore the function of Tangnaikang (TNK) in the prevention and treatment of renal interstitial fibrosis through transdifferentiation of the human renal tubular epithelial cell line HK-2 induced by transforming growth factor-β1(TGF-β1).METHODS: HK-2 cells cultured in dulbecco’s modified eagle medium/F12 (1∶1) with 10% fetal calf serum were divided into six groups: blank control group, TGF-β1 group (TGF-β1 10 ng/mL), serum control group (TGF-β1 10 ng/mL+10% serum), treatment group 1 (TGF-β1 10 ng/mL+ 5% TNK serum),treatment group 2 (TGF-β1 10 ng/mL+10% TNK serum), and treatment group 3 (TGF-β1 10 ng/mL+20% TNK serum). Cell proliferation was detected by 4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Expression of α-smooth muscle actin (α-SMA) and E-cadherin were observed by immunohistochemical assay. The contents of collagen Ⅰ (Col Ⅰ), collagen Ⅲ (Col Ⅲ), and fibronectin (FN) in the culture medium supernatant were detected by ELISA.RESULTS: E-cadherin was expressed and α-SMA was not expressed in normal HK-2 cells. In HK-2 cells cultured with TGF-β1,α-SMA expression significantly increased, HK-2 cells significantly proliferated, and secretion of Col Ⅰ, Col Ⅲ, and FN significantly increased compared with the blank control group (all P<0.05). In the HK-2 cells cultured with TGF-β1 and TNK serum, the expression of α-SMA significantly decreased, the expression of E-cadherin significantly increased, and the cell proliferation and the secretion of Col Ⅰ, Col Ⅲ and FN were significantly inhibited compared with the TGF-β1 group (all P<0.05).CONCLUSION: TNK can inhibit cell proliferation and reduce secretion of Col Ⅰ, Col Ⅲ, and FN.This indicates that TNK can inhibit transdifferentiation of human renal tubular epithelial cells induced by TGF-β1, with the effect of preventing and treating renal interstitial fibrosis. OBJECTIVE: To explore the function of Tangnaikang (TNK) in the prevention and treatment of renal interstitial fibrosis through transdifferentiation of the human renal tubular epithelial cell line HK-2 induced by transforming growth factor- β1 (TGF-β1). METHODS: HK- 2 cells cultured in dulbecco’s modified eagle medium / F12 (1: 1) with 10% fetal calf serum were divided into six groups: blank control group, TGF-β1 group (TGF-β1 10 ng / treatment group 1 (TGF-β1 10 ng / mL + 5% TNK serum), treatment group 2 (TGF-β1 10 ng / mL + 10% 3 (TGF-β1 10 ng / mL + 20% TNK serum). Expression of α-smooth muscle actin (α- SMA) and E-cadherin were observed by immunohistochemical assay. The contents of collagen Ⅰ (Col Ⅰ), collagen Ⅲ (Col Ⅲ), and fibronectin (FN) in the culture medium supernatant were detected by ELISA.RESU In HK-2 cells cultured with TGF-β1, α-SMA expression significantly increased, HK-2 cells significantly proliferated, and secretion of Col (All P <0.05). In the HK-2 cells cultured with TGF-β1 and TNK serum, the expression of α-SMA significantly decreased, the expression of E -cadherin significantly increased, and the cell proliferation and the secretion of Col Ⅰ, Col Ⅲ and FN were significantly inhibited compared with the TGF-β1 group (all P <0.05) .CONCLUSION: TNK can inhibit cell proliferation and reduce secretion of Col Ⅰ , Col III, and FN.This indicates that TNK can inhibit trans-differentiation of human renal tubular epithelial cells induced by TGF-β1, with the effect of preventing and treating renal interstitial fibrosis.