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Procyanidin B2 inhibits high glucose-induced epithelial-mesenchymal transition in HK-2 human renal proximal tubular epithelial cells

Diabetic nephropathy (DN) is not only an important chronic complication of diabetes, but is also one of the predominant cause of renal failure. Previous studies have indicated that the process termed 'epithelial-mesenchymal transition' (EMT) results in fibrosis of renal tubular epithelial cells, and... Full description

Journal Title: Molecular Medicine Reports 12/2015, Vol.12(6), pp.8148-8154
Main Author: Li, Dandan
Other Authors: Zhao, Tingbao , Meng, Jianzhong , Jing, Ying , Jia, Fengyu , He, Ping
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 1791-2997 ; E-ISSN: 1791-3004 ; DOI: 10.3892/mmr.2015.4445
Link: http://www.spandidos-publications.com/molecular medicine reports/12/6/8148
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recordid: spandido10.3892/mmr.2015.4445
title: Procyanidin B2 inhibits high glucose-induced epithelial-mesenchymal transition in HK-2 human renal proximal tubular epithelial cells
format: Article
creator:
  • Li, Dandan
  • Zhao, Tingbao
  • Meng, Jianzhong
  • Jing, Ying
  • Jia, Fengyu
  • He, Ping
subjects:
  • Procyanidin B2
  • Epithelial-Mesenchymal Transition
  • Hk-2
  • Transforming Growth Factor-Β/Small Mothers Against Decapentaplegic
  • Mitogen-Activated Protein Kinase/P38
ispartof: Molecular Medicine Reports, 12/2015, Vol.12(6), pp.8148-8154
description: Diabetic nephropathy (DN) is not only an important chronic complication of diabetes, but is also one of the predominant cause of renal failure. Previous studies have indicated that the process termed 'epithelial-mesenchymal transition' (EMT) results in fibrosis of renal tubular epithelial cells, and is key in DN. As an antioxidant, procyanidin B2 can inhibit cardiac fibrosis; however, whether it has an effect on the inhibition of renal fibrosis remains to be elucidated. The present study demonstrated that high glucose levels were able to activate EMT-associated changes, including the loss of E-cadherin and increase in α-smooth muscle actin (α-SMA), as determined by western blotting and immunofluorescence. Pre-treatment with procyanidin B2 reversed the high glucose-induced morphological changes, upregulated the expression of E-cadherin and downregulated the expression levels of vimentin and α-SMA. Furthermore, procyanidin B2 decreased the phosphorylation of small mothers against decapentaplegic (Smad)2, Smad3 and P38, and upregulated the expression of phosphorylated-Smad7. In conclusion, the results of the present study suggested that procyanidin B2 inhibited high glucose-induced EMT through the inhibition of transforming growth factor-β/Smad and mitogen-activated protein kinase/P38 signaling pathways.
language: eng
source:
identifier: ISSN: 1791-2997 ; E-ISSN: 1791-3004 ; DOI: 10.3892/mmr.2015.4445
fulltext: fulltext
issn:
  • 1791-2997
  • 17912997
  • 1791-3004
  • 17913004
url: Link


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titleProcyanidin B2 inhibits high glucose-induced epithelial-mesenchymal transition in HK-2 human renal proximal tubular epithelial cells
creatorLi, Dandan ; Zhao, Tingbao ; Meng, Jianzhong ; Jing, Ying ; Jia, Fengyu ; He, Ping
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subjectProcyanidin B2 ; Epithelial-Mesenchymal Transition ; Hk-2 ; Transforming Growth Factor-Β/Small Mothers Against Decapentaplegic ; Mitogen-Activated Protein Kinase/P38
descriptionDiabetic nephropathy (DN) is not only an important chronic complication of diabetes, but is also one of the predominant cause of renal failure. Previous studies have indicated that the process termed 'epithelial-mesenchymal transition' (EMT) results in fibrosis of renal tubular epithelial cells, and is key in DN. As an antioxidant, procyanidin B2 can inhibit cardiac fibrosis; however, whether it has an effect on the inhibition of renal fibrosis remains to be elucidated. The present study demonstrated that high glucose levels were able to activate EMT-associated changes, including the loss of E-cadherin and increase in α-smooth muscle actin (α-SMA), as determined by western blotting and immunofluorescence. Pre-treatment with procyanidin B2 reversed the high glucose-induced morphological changes, upregulated the expression of E-cadherin and downregulated the expression levels of vimentin and α-SMA. Furthermore, procyanidin B2 decreased the phosphorylation of small mothers against decapentaplegic (Smad)2, Smad3 and P38, and upregulated the expression of phosphorylated-Smad7. In conclusion, the results of the present study suggested that procyanidin B2 inhibited high glucose-induced EMT through the inhibition of transforming growth factor-β/Smad and mitogen-activated protein kinase/P38 signaling pathways.
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descriptionDiabetic nephropathy (DN) is not only an important chronic complication of diabetes, but is also one of the predominant cause of renal failure. Previous studies have indicated that the process termed 'epithelial-mesenchymal transition' (EMT) results in fibrosis of renal tubular epithelial cells, and is key in DN. As an antioxidant, procyanidin B2 can inhibit cardiac fibrosis; however, whether it has an effect on the inhibition of renal fibrosis remains to be elucidated. The present study demonstrated that high glucose levels were able to activate EMT-associated changes, including the loss of E-cadherin and increase in α-smooth muscle actin (α-SMA), as determined by western blotting and immunofluorescence. Pre-treatment with procyanidin B2 reversed the high glucose-induced morphological changes, upregulated the expression of E-cadherin and downregulated the expression levels of vimentin and α-SMA. Furthermore, procyanidin B2 decreased the phosphorylation of small mothers against decapentaplegic (Smad)2, Smad3 and P38, and upregulated the expression of phosphorylated-Smad7. In conclusion, the results of the present study suggested that procyanidin B2 inhibited high glucose-induced EMT through the inhibition of transforming growth factor-β/Smad and mitogen-activated protein kinase/P38 signaling pathways.
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abstractDiabetic nephropathy (DN) is not only an important chronic complication of diabetes, but is also one of the predominant cause of renal failure. Previous studies have indicated that the process termed 'epithelial-mesenchymal transition' (EMT) results in fibrosis of renal tubular epithelial cells, and is key in DN. As an antioxidant, procyanidin B2 can inhibit cardiac fibrosis; however, whether it has an effect on the inhibition of renal fibrosis remains to be elucidated. The present study demonstrated that high glucose levels were able to activate EMT-associated changes, including the loss of E-cadherin and increase in α-smooth muscle actin (α-SMA), as determined by western blotting and immunofluorescence. Pre-treatment with procyanidin B2 reversed the high glucose-induced morphological changes, upregulated the expression of E-cadherin and downregulated the expression levels of vimentin and α-SMA. Furthermore, procyanidin B2 decreased the phosphorylation of small mothers against decapentaplegic (Smad)2, Smad3 and P38, and upregulated the expression of phosphorylated-Smad7. In conclusion, the results of the present study suggested that procyanidin B2 inhibited high glucose-induced EMT through the inhibition of transforming growth factor-β/Smad and mitogen-activated protein kinase/P38 signaling pathways.
pubD.A. Spandidos
doi10.3892/mmr.2015.4445
date2015-12