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Exp Cell Res. 2014 May 1;323(2):255-62. doi: 10.1016/j.yexcr.2014.01.028. Epub 2014 Feb 10.

The effects of diosgenin in the regulation of renal proximal tubular fibrosis.

Author information

1
Graduate Institute of Biomedical Science, Chung Hwa University of Medical Technology, Tainan, Taiwan.
2
Graduate Institute of Biomedical Science, Chung Hwa University of Medical Technology, Tainan, Taiwan; 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
Graduate Institute of Biomedical Science, Chung Hwa University of Medical Technology, Tainan, Taiwan; Department of Public Health, National Taiwan University, Taipei, Taiwan.
6
Graduate Institute of Biomedical Science, Chung Hwa University of Medical Technology, Tainan, Taiwan; Department of Medical Laboratory Science and Biotechnology, Chung Hwa University of Medical Technology, Tainan, Taiwan. Electronic address: Call0955443221@gmail.com.

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, 27.5mM) 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.

KEYWORDS:

Epithelial-to-mesenchymal transition; Glucose; Renal tubular fibrosis

PMID:
24525371
DOI:
10.1016/j.yexcr.2014.01.028
[Indexed for MEDLINE]

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