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Plos One : Norcantharidin Inhibits Renal Interstitial Fibrosis by Blocking the Tubular Epithelial-mesenchymal Transition, Volume 8

By Burdmann, Emmanuel, A

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Book Id: WPLBN0003963976
Format Type: PDF eBook :
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Reproduction Date: 2015

Title: Plos One : Norcantharidin Inhibits Renal Interstitial Fibrosis by Blocking the Tubular Epithelial-mesenchymal Transition, Volume 8  
Author: Burdmann, Emmanuel, A
Volume: Volume 8
Language: English
Subject: Journals, Science, Medical Science
Collections: Periodicals: Journal and Magazine Collection (Contemporary)
Historic
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Publisher: Plos

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Burdmann, E. A. (n.d.). Plos One : Norcantharidin Inhibits Renal Interstitial Fibrosis by Blocking the Tubular Epithelial-mesenchymal Transition, Volume 8. Retrieved from http://www.worldlibrary.org/


Description
Description : Epithelial–mesenchymal transition (EMT) is thought to contribute to the progression of renal tubulointerstitial fibrosis. Norcantharidin (NCTD) is a promising agent for inhibiting renal interstitial fibrosis. However, the molecular mechanisms of NCTD are unclear. In this study, a unilateral ureteral obstruction (UUO) rat model was established and treated with intraperitoneal NCTD (0.1 mg/kg/day). The UUO rats treated with NCTD showed a reduction in obstruction-induced upregulation of a-SMA and downregulation of E-cadherin in the rat kidney (P,0.05). Human renal proximal tubule cell lines (HK-2) stimulated with TGF-b1 were treated with different concentrations of NCTD. HK-2 cells stimulated by TGF-b1 in vitro led to downregulation of E-cadherin and increased de novo expression of a-SMA: co-treatment with NCTD attenuated all of these changes (P,0.05). NCTD reduced TGF-b1-induced expression and phosphorylation of Smad2/3 and downregulated the expression of Snail1 (P,0.05). These results suggest that NCTD antagonizes tubular EMT by inhibiting the Smad pathway. NCTD may play a critical role in preserving the normal epithelial phenotype and modulating tubular EMT.

 

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