Abstract: Objective To investigate the effect and mechanism of emodin (EM) on TGF- β1-induced epithelialmesenchymal transition and the expression of mitofusin 2 (Mfn2) in human renal tubular epithelial cells (HK-2). Methods CCK-8 was used to detect the effects of different concentrations of emodin on the proliferation of HK-2 cells. The experiment cells were divided into blank control group, TGF-β1 group and TGF-β1+EM group. The emodin intervention group was treated with different concentrations of emodin (10, 20 and 40 μmol/L) for 30 min, and the TGF-β1 group and the emodin intervention group were simultaneously stimulated with TGF- β1 at a concentration of 10 μg/L for 48 h. The cells were then harvested and the expressions of α-smooth muscle actin (α-SMA), E-cadherin, connective tissue growth factor (CTGF) and Mfn2 proteins were detected by Western blot assay. Results The CCK-8 result suggested that the survival rate(% ) of HK-2 cells were 100.00±0.00, 90.89±2.17, 88.52±1.67, 87.72±2.00, 63.46±1.73 and 52.19±2.60 in the EM treatment groups at 0, 10, 20, 40, 80, and 160 μmol/L concentrations, showing a gradually decreasing trend (P＜0.01).Western blot results showed that the protein levels of α-SMA, CTGF and Mfn2 increased in HK-2 cells, and the expression of E-cadherin protein decreased after stimulation with TGF-β1 compared with those of the blank control group (P＜0.05).Compared with the TGF- β1 group, α -SMA, CTGF and Mfn2 protein levels were decreased, and E-cadherin protein expression was increased after treatment with different concentrations of emodin (P＜0.05) in a dose-dependent manner. Conclusion Emodin attenuates TGF- β1-induced epithelial-mesenchymal transition in human renal tubular epithelial cells, which may ameliorate renal fibrosis by reducing the expression of TGF-β1-induced Mfn2.

Key words: emodin, transforming growth factor β1, epithelial-mesenchymal transition, mitofusin2, renal fibrosis