Arginyl-fructosyl-glucose from red ginseng alleviates TGF-β1-induced epithelial-mesenchymal transition of renal tubular epithelial cells

This study aims to explore the effect and mechanism of arginyl-fructosyl-glucose (AFG) on TGF-beta 1-induced epithelial-mesenchymal transition (EMT) of renal tubular epithelial cells. HK-2 cells were induced by TGF-beta 1 and then co-cultured with AFG at different concentrations (0, 25, 50, and 100 mu mol/l) for 48 h. The morphology of HK-2 cells was observed under an inverted microscope and the expressions of alpha-SMA, Vimentin, and E-cadherin were assessed by qRT-PCR, Western blot, and immunofluorescencc. The mRNA expressions of ERK and STAT3 were also examined by qRT-PCR, and the protein levels of ERK, STAT3, p-ERK, and p-STAT3 were measured by Western blot. Finally, CCK-8 and transwell assays were used to detect cell proliferation and invasion. TGF-beta 1 treatment significantly induced EMT in HK-2 cells. The expressions of p-ERK and p-STAT3 were signally increased after TGF-beta 1 induction, while Mogrol treatment inhibited p-ERK, p-STAT3, alpha-SMA, and Vimentin expression levels, enhanced E-cadherin expression, and suppressed cell proliferation and invasion. AFG exposure could also inhibit p-ERK, p-STAT3, alpha-SMA, and Vimentin expressions, promote E-cadherin expression, and markedly inhibit HK-2 cell proliferation and invasion. AFG inhibited TGF-beta 1-induced EMT of renal tubular epithelial cells by regulating phosphorylation of ERK and STAT3.