Fig 1: TG inhibits podocyte epithelial-mesenchymal transition and apoptosis through the mTOR/Twist1 signaling pathway. (A) Immunofluorescence of vimentin and LC3II (scale bar, 20 µm; magnification, ×400). (B) Semi-quantitative evaluation of vimentin and LC3II, as determined by immunofluorescence. Control values were set at 1. (C) Representative western blots of p-mTOR, LC3, p62, Twist1, E-cadherin and N-cadherin expression in the different groups. (D) Densitometric analysis of p-mTOR/mTOR, LC3II/I, p62, Twist1, E-cadherin and N-cadherin expression from different groups, as determined by western blotting. (E) Cellular apoptosis in each group was detected by flow cytometry. (F) Apoptotic rates in each group. Control, cells treated with serum from control mice (C57BLKS/J db/m) for 24 h; DKD, cells treated with serum from DKD mice (C57BLKS/J db/db) for 24 h; DKD + TG, cells treated with serum from DKD mice (C57BLKS/J db/db) for 24 h, and then treated with 1.25 µg/ml TG for 72 h; DKD + TG + 3BDO, cells treated with serum from DKD mice (C57BLKS/J db/db) for 24 h and 1.25 µg/ml TG for 72 h, and then incubated with 60 µM 3BDO for 24 h. Data analysis was performed by one-way ANOVA followed by Tukey's post-hoc test. Data are presented as the mean ± standard deviation. *P<0.05, **P<0.01. TG, tripterygium glycoside; p-, phosphorylated; LC3, microtubule-associated protein 1 light chain 3; DKD, diabetic kidney disease; 3BDO, 3-benzyl-5-((2-nitrophenoxy) methyl)-dihydrofuran-2(3H)-one.