Allicin inhibits tubular epithelial-myofibroblast transdifferentiation under high glucose conditions in vitro.

摘要: Previous studies have suggested that tubular epithelial-mesenchymal transition (EMT) is an important event in renal tubulointerstitial fibrosis, which a clinical characteristic of diabetic nephropathy. The present study aimed to investigate the effect allicin, major biological active component garlic, on EMT human proximal epithelial cell line (HK-2) cultured under high glucose concentrations. HK-2 cells were exposed for 48 h 5.5 or 25 mmol/l D-glucose, D-glucose plus allicin (2.5, 5, 10 20 µg/ml) µmol/l PD98059, selective inhibitor mitogen activated protein kinase/extracellular signal-regulated kinase (ERK) signaling pathway. was assessed by analyzing expression E-cadherin, α-smooth muscle actin (α-SMA), vimentin and collagen I via immunocytochemistry. In addition, reverse transcription-quantitative polymerase chain reaction western blotting used detect levels transforming growth factor (TGF)-β1 phosphorylated (p)-ERK1/2. Marked morphological changes observed conditions, these abrogated simultaneous incubation with PD98059. α-SMA, significantly increased as compared those normal conditions (P<0.01). Conversely, E-cadherin decreased upon stimulation Furthermore, TGF-β1 p-ERK1/2 upregulated (P<0.05). Allicin partially reversed high-glucose-induced increase (P<0.01 at µg/ml), downregulated glucose-induced dose-dependent manner results concentrations induced cells, able inhibit EMT, potentially regulation ERK1/2-TGF-β1