The effects of diosgenin in the Regulation of renal proximal tubular fibrosis |
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Authors: | Wei-Cheng Wang Shu-Fen Liu Wen-Teng Chang Yow-Ling Shiue Pei-fang Hsieh Tsung-Jen Hung Chien-Ya Hung Yu-Ju Hung Mei-Fen Chen Yu-Lin Yang |
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Institution: | 1. Graduate Institute of Biomedical Science, Chung Hwa University of Medical Technology, Tainan, Taiwan;2. Department of Internal Medicine, Kaohsiung Medical University Chung-Ho Memorial Hospital, Kaohsiung, Taiwan;3. Graduate Institute of Biomedical Science, National Sun Yat-sen University, Kaohsiung, Taiwan;4. Department of Food nutrition, Chung Hwa University of Medical Technology, Tainan, Taiwan;5. Department of Public Health, National Taiwan University, Taipei, Taiwan;6. Department of Medical Laboratory Science and Biotechnology, Chung Hwa University of Medical Technology, Tainan, Taiwan |
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Abstract: | Fibrosis is the important pathway for end-stage renal failure. Glucose has been demonstrated to be the most important fibrogenesis-inducing agent according to previous studies. Despite diosgenin has been demonstrated to be anti-inflammatory, the possible role in fibrosis regulation of diosgenin remain to be investigated. In this study, renal proximal tubular epithelial cells (designated as HK-2) were treated with high concentration of glucose (HG, 27.5 mM) to determine whether diosgenin (0.1, 1 and 10 μM) has the effects to regulate renal cellular fibrosis. We found that 10 μM of diosgenin exert optimal inhibitory effects on high glucose-induced fibronectin expression in HK-2 cells. In addition, diosgenin markedly inhibited HG-induced increase in α-smooth muscle actin (α-SMA) and HG-induced decrease in E-cadherin. In addition, diosgenin antagonizes high glucose-induced epithelial-to-mesenchymal transition (EMT) signals partly by enhancing the catabolism of Snail in renal cells. Collectively, these data suggest that diosgenin has the potential to inhibit high glucose-induced renal tubular fibrosis possibly through EMT pathway. |
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Keywords: | Glucose Renal tubular fibrosis Epithelial-to-mesenchymal transition |
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