Effect of Tangnaikang on TGF-β1-induced transdifferentiation of human renal tubular epithelial HK-2 cells
Journal Articles
Overview
Research
Identity
Additional Document Info
View All
Overview
abstract
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-beta1 (TGF-beta1). 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-beta1 group (TGF-beta1 10 ng/mL), serum control group (TGF-beta1 10 ng/mL + 10% serum), treatment group 1 (TGF-beta1 10 ng/mL + 5% TNK serum), treatment group 2 (TGF-beta1 10 ng/mL + 10% TNK serum), and treatment group 3 (TGF-beta1 10 ng/mL + 20% TNK serum). Cell proliferation was detected by 4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Expression of alpha-smooth muscle actin (alpha-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 alpha-SMA was not expressed in normal HK-2 cells. In HK-2 cells cultured with TGF-beta1, alpha-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-beta1 and TNK serum, the expression of alpha-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-beta1 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-beta1, with the effect of preventing and treating renal interstitial fibrosis.
