ObjectiveTo observe the influence of hepatocyte growth-promoting factor (pHGF) on monocyte chemotatic protein-1-(MCP-1) and aristolochic acid Ⅰ(AAⅠ)-induced epithelial-to-mesenchymal transition (EMT) and apoptosis of human kidney epithelial cell line(HKC).MethodsThe HKC cells were randomly divided into blank control group (control groups), epithelial-to-mesenchymal transition model group (model group),and pHGF inhibition group (pHGF groups) with pHGF at different concentrations (0.15,1.5,15,150,and 1 500 ng/ml).The EMT model was established by exposing HKC cells to MCP-1(0.1 μg/ml)and AAⅠ(10 μg/ml).Cells in the pHGF groups were the model cells treated with different concentrations of pHGF.Cells in the control group were cultured routinely.WST-8 method and flow cytometry were used to observe the proliferation and apoptosis of HKC cells,respectively.The mRNA expression of α-smooth muscle actin(α-SMA) was determined by reverse transcriptase-polymerase chain reaction(RT-PCR),and the expression of α-SMA,fibronectin (FN),and transforming growth factor-β1(TGF-β1) in HKC cells were assessed by indirect enzyme immunohistochemistry.ResultsThe cell inhibitory rate,apoptotic rate,and expression of α-SMA mRNA were significantly increased in the model group and pHGF groups compared with those in the control group (P<0.01),indicating the successful establishment of EMT model.Compared with the model group,pHGF at 150 ng/ml,but not at other concentrations,significantly decreased the inhibition rate of HKC cells(P<0.01).The apoptotic rate of HKC cells in all the pHGF groups were significantly lower than that in the model group (P<0.01).pHGF at 150 ng/ml also greatly decreased the expression of α-SMA mRNA,and significantly down-regulated the expression of α-SMA,TGF-β1,and FN protein.ConclusionpHGF at 150 ng/ml can partly reverse MCP-1- and AA Ⅰ-induced HKC cell growth inhibition,apoptosis,and EMT.