کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10904049 | 1086554 | 2014 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The effects of diosgenin in the Regulation of renal proximal tubular fibrosis
ترجمه فارسی عنوان
اثرات دیوسژنین در تنظیم فیبروز تومور پروگزیمال کلیه
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کلمات کلیدی
گلوکز، فیبروز لوله ای کلیه، گذار اپیتلیال به مزانشیمال،
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
چکیده انگلیسی
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.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Cell Research - Volume 323, Issue 2, 1 May 2014, Pages 255-262
Journal: Experimental Cell Research - Volume 323, Issue 2, 1 May 2014, Pages 255-262
نویسندگان
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,