Salvianolic acid B prevents epithelial-to-mesenchymal transition through the TGF-β1 signal transduction pathway <it>in vivo </it>and <it>in vitro</it>
<p>Abstract</p> <p>Background</p> <p>Salvianolic Acid B (Sal B) is a water-soluble component from Danshen (a traditional Chinese herb widely used for chronic renal diseases) with anti-oxidative and cell protective properties. Sal B also has potential protective effects...
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doaj-e60e572f307d49d6ab306bc00521231e2020-11-24T21:21:54ZengBMCBMC Cell Biology1471-21212010-05-011113110.1186/1471-2121-11-31Salvianolic acid B prevents epithelial-to-mesenchymal transition through the TGF-β1 signal transduction pathway <it>in vivo </it>and <it>in vitro</it>Yuan Ji-LiTao Yan-YanWang Qing-LanShen LiLiu Cheng-Hai<p>Abstract</p> <p>Background</p> <p>Salvianolic Acid B (Sal B) is a water-soluble component from Danshen (a traditional Chinese herb widely used for chronic renal diseases) with anti-oxidative and cell protective properties. Sal B also has potential protective effects on renal diseases. Tubular epithelial cells can undergo epithelial-to-mesenchymal transition (EMT), which plays an important role in the pathogenesis of renal interstitial fibrosis (RIF) and is mainly regulated by TGF-β1/Smads pathway. The aims of the study are to investigate the effect of Sal B on tubular EMT <it>in vivo </it>and <it>in vitro</it>, and to elucidate its underlying mechanism against EMT related to TGF-β1/Smads pathway.</p> <p>Results</p> <p>For <it>in vivo </it>experiments, RIF was induced in rats by oral administration of HgCl<sub>2 </sub>and prophylaxised with Sal B and vitamin E. The protein expression of E-cadherin was down-regulated, while the expression of α-SMA, TGF-β1, TβR-I, p-Smad2/3 and the activity of matrix metalloproteinase-2 (MMP-2) were up-regulated in kidneys of model rats when compared with those of normal rats. In contrast, Sal B and vitamin E significantly attenuated the expression of α-SMA, TGF-β1, TβR-I, p-Smad2/3, and MMP-2 activity, but increased E-cadherin expression. For <it>in vitro </it>experiments, HK-2 cells were incubated with TGF-β1 to induce EMT, and the cells were co-cultured with 1 and 10 μM Sal B or SB-431542 (a specific inhibitor of TβR-I kinase). TGF-β1 induced a typical EMT in HK-2 cells, while it was blocked by Sal B and SB-431542, as evidenced by blocking morphologic transformation, restoring E-cadherin and CK-18 expression, inhibiting α-SMA expression and F-actin reorganization, and down-regulating MMP-2/9 activities in TGF-β1 mediated HK-2 cells. Furthermore, Sal B and SB-431542 profoundly down-regulated the expressions of TβR-I and p-Smad2/3 but prevented the decreased expression of Smad7 in TGF-β1 stimulated HK-2 cells.</p> <p>Conclusions</p> <p>Sal B can prevent tubular EMT in the fibrotic kidney induced by HgCl<sub>2 </sub>as well as HK-2 cells triggered by TGF-β1, the mechanism of Sal B is closely related to the regulation of TGF-β1/Smads pathway, manifested as the inhibition of TGF-β1 expression, suppression of TβR-I expression and function, down-regulation of Smad2/3 phosphorylation, and restoration of the down-regulation of Smad7, as well as inhibition of MMP-2 activity.</p> http://www.biomedcentral.com/1471-2121/11/31 |
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DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Yuan Ji-Li Tao Yan-Yan Wang Qing-Lan Shen Li Liu Cheng-Hai |
spellingShingle |
Yuan Ji-Li Tao Yan-Yan Wang Qing-Lan Shen Li Liu Cheng-Hai Salvianolic acid B prevents epithelial-to-mesenchymal transition through the TGF-β1 signal transduction pathway <it>in vivo </it>and <it>in vitro</it> BMC Cell Biology |
author_facet |
Yuan Ji-Li Tao Yan-Yan Wang Qing-Lan Shen Li Liu Cheng-Hai |
author_sort |
Yuan Ji-Li |
title |
Salvianolic acid B prevents epithelial-to-mesenchymal transition through the TGF-β1 signal transduction pathway <it>in vivo </it>and <it>in vitro</it> |
title_short |
Salvianolic acid B prevents epithelial-to-mesenchymal transition through the TGF-β1 signal transduction pathway <it>in vivo </it>and <it>in vitro</it> |
title_full |
Salvianolic acid B prevents epithelial-to-mesenchymal transition through the TGF-β1 signal transduction pathway <it>in vivo </it>and <it>in vitro</it> |
title_fullStr |
Salvianolic acid B prevents epithelial-to-mesenchymal transition through the TGF-β1 signal transduction pathway <it>in vivo </it>and <it>in vitro</it> |
title_full_unstemmed |
Salvianolic acid B prevents epithelial-to-mesenchymal transition through the TGF-β1 signal transduction pathway <it>in vivo </it>and <it>in vitro</it> |
title_sort |
salvianolic acid b prevents epithelial-to-mesenchymal transition through the tgf-β1 signal transduction pathway <it>in vivo </it>and <it>in vitro</it> |
publisher |
BMC |
series |
BMC Cell Biology |
issn |
1471-2121 |
publishDate |
2010-05-01 |
description |
<p>Abstract</p> <p>Background</p> <p>Salvianolic Acid B (Sal B) is a water-soluble component from Danshen (a traditional Chinese herb widely used for chronic renal diseases) with anti-oxidative and cell protective properties. Sal B also has potential protective effects on renal diseases. Tubular epithelial cells can undergo epithelial-to-mesenchymal transition (EMT), which plays an important role in the pathogenesis of renal interstitial fibrosis (RIF) and is mainly regulated by TGF-β1/Smads pathway. The aims of the study are to investigate the effect of Sal B on tubular EMT <it>in vivo </it>and <it>in vitro</it>, and to elucidate its underlying mechanism against EMT related to TGF-β1/Smads pathway.</p> <p>Results</p> <p>For <it>in vivo </it>experiments, RIF was induced in rats by oral administration of HgCl<sub>2 </sub>and prophylaxised with Sal B and vitamin E. The protein expression of E-cadherin was down-regulated, while the expression of α-SMA, TGF-β1, TβR-I, p-Smad2/3 and the activity of matrix metalloproteinase-2 (MMP-2) were up-regulated in kidneys of model rats when compared with those of normal rats. In contrast, Sal B and vitamin E significantly attenuated the expression of α-SMA, TGF-β1, TβR-I, p-Smad2/3, and MMP-2 activity, but increased E-cadherin expression. For <it>in vitro </it>experiments, HK-2 cells were incubated with TGF-β1 to induce EMT, and the cells were co-cultured with 1 and 10 μM Sal B or SB-431542 (a specific inhibitor of TβR-I kinase). TGF-β1 induced a typical EMT in HK-2 cells, while it was blocked by Sal B and SB-431542, as evidenced by blocking morphologic transformation, restoring E-cadherin and CK-18 expression, inhibiting α-SMA expression and F-actin reorganization, and down-regulating MMP-2/9 activities in TGF-β1 mediated HK-2 cells. Furthermore, Sal B and SB-431542 profoundly down-regulated the expressions of TβR-I and p-Smad2/3 but prevented the decreased expression of Smad7 in TGF-β1 stimulated HK-2 cells.</p> <p>Conclusions</p> <p>Sal B can prevent tubular EMT in the fibrotic kidney induced by HgCl<sub>2 </sub>as well as HK-2 cells triggered by TGF-β1, the mechanism of Sal B is closely related to the regulation of TGF-β1/Smads pathway, manifested as the inhibition of TGF-β1 expression, suppression of TβR-I expression and function, down-regulation of Smad2/3 phosphorylation, and restoration of the down-regulation of Smad7, as well as inhibition of MMP-2 activity.</p> |
url |
http://www.biomedcentral.com/1471-2121/11/31 |
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