Effect of Tangnaikang on TGF-β1-induced transdifferentiation of human renal tubular epithelial HK-2 cells

Abstract

ObjectiveTo 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). MethodsHK-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. ResultsE-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). ConclusionTNK 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.