The effects of diosgenin in the Regulation of renal proximal tubular fibrosis

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• 作者：Wei-Cheng Wang^a ; Shu-Fen Liu^a ; ^b ; Wen-Teng Chang^a ; Yow-Ling Shiue^c ; Pei-fang Hsieh^c ; Tsung-Jen Hung^a ; Chien-Ya Hung^d ; Yu-Ju Hung^a ; ^e ; Mei-Fen Chen^a ; Yu-Lin Yang^a ; ^f ; ^{Call0955443221@gmail.com" class="auth_mail}
• 关键词：Glucose ; Renal tubular fibrosis ; Epithelial-to-mesenchymal transition
• 刊名：Experimental Cell Research
• 出版年：1 May, 2014
• 年：2014
• 卷：323
• 期：2
• 页码：255-262
• 全文大小：2812 K

文摘

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 渭M) has the effects to regulate renal cellular fibrosis. We found that 10 渭M 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 伪-smooth muscle actin (伪-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.