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Ferulic Acid Attenuates TGF-β1-Induced Renal Cellular Fibrosis in NRK-52E Cells by Inhibiting Smad/ILK/Snail Pathway.

Abstract

Renal fibrosis is a common cause of renal dysfunction with chronic kidney disease. Central to this process is epithelial-mesenchymal transformation (EMT) of proximal tubular epithelial cells driven by transforming growth factor-β1 (TGF-β1) signaling. The present study aimed to investigate the effect of Ferulic acid (FA) on EMT of renal proximal tubular epithelial cell line (NRK-52E) induced by TGF-β1 and to elucidate its underlying mechanism against EMT related to TGF-β1/Smads pathway. The NRK-52E cells were treated for 48 h with TGF-β1 (5 ng/mL) in different concentrations of FA (0 to 200 µM). Fibronectin, a mesenchymal marker, was assessed by western blotting. Western blotting was also used to examine the EMT markers (E-cadherin, and α-smooth muscle actin (α-SMA)), signal transducer (p-Smad2/3), and EMT initiator (Snail). ILK was also assayed by western blotting. The results showed that TGF-β1 induced spindle-like morphological transition in NRK-52E cells. Smad2/3 signaling pathway activation, increased fibronectin, α-SMA, ILK, and Snail expression, and decreased E-cadherin expression in TGF-β1-treated NRK-52E cells. FA efficiently blocked P-Smad2/3 activation and attenuated all these EMT changes induced by TGF-β1. These findings suggest that FA may serve as a potential fibrosis antagonist for renal proximal tubule cells by inhibiting EMT process.

Authors+Show Affiliations

The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, China.Jiangsu Province Hospital of Traditional Chinese Medicine, Nanjing, Jiangsu 210029, China.Jiangsu Province Hospital of Traditional Chinese Medicine, Nanjing, Jiangsu 210029, China.The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, China.The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

25949265

Citation

Wei, Ming-Gang, et al. "Ferulic Acid Attenuates TGF-β1-Induced Renal Cellular Fibrosis in NRK-52E Cells By Inhibiting Smad/ILK/Snail Pathway." Evidence-based Complementary and Alternative Medicine : ECAM, vol. 2015, 2015, p. 619720.
Wei MG, Sun W, He WM, et al. Ferulic Acid Attenuates TGF-β1-Induced Renal Cellular Fibrosis in NRK-52E Cells by Inhibiting Smad/ILK/Snail Pathway. Evid Based Complement Alternat Med. 2015;2015:619720.
Wei, M. G., Sun, W., He, W. M., Ni, L., & Yang, Y. Y. (2015). Ferulic Acid Attenuates TGF-β1-Induced Renal Cellular Fibrosis in NRK-52E Cells by Inhibiting Smad/ILK/Snail Pathway. Evidence-based Complementary and Alternative Medicine : ECAM, 2015, 619720. https://doi.org/10.1155/2015/619720
Wei MG, et al. Ferulic Acid Attenuates TGF-β1-Induced Renal Cellular Fibrosis in NRK-52E Cells By Inhibiting Smad/ILK/Snail Pathway. Evid Based Complement Alternat Med. 2015;2015:619720. PubMed PMID: 25949265.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Ferulic Acid Attenuates TGF-β1-Induced Renal Cellular Fibrosis in NRK-52E Cells by Inhibiting Smad/ILK/Snail Pathway. AU - Wei,Ming-Gang, AU - Sun,Wei, AU - He,Wei-Ming, AU - Ni,Li, AU - Yang,Yan-Yu, Y1 - 2015/04/08/ PY - 2015/01/19/received PY - 2015/03/18/accepted PY - 2015/5/8/entrez PY - 2015/5/8/pubmed PY - 2015/5/8/medline SP - 619720 EP - 619720 JF - Evidence-based complementary and alternative medicine : eCAM JO - Evid Based Complement Alternat Med VL - 2015 N2 - Renal fibrosis is a common cause of renal dysfunction with chronic kidney disease. Central to this process is epithelial-mesenchymal transformation (EMT) of proximal tubular epithelial cells driven by transforming growth factor-β1 (TGF-β1) signaling. The present study aimed to investigate the effect of Ferulic acid (FA) on EMT of renal proximal tubular epithelial cell line (NRK-52E) induced by TGF-β1 and to elucidate its underlying mechanism against EMT related to TGF-β1/Smads pathway. The NRK-52E cells were treated for 48 h with TGF-β1 (5 ng/mL) in different concentrations of FA (0 to 200 µM). Fibronectin, a mesenchymal marker, was assessed by western blotting. Western blotting was also used to examine the EMT markers (E-cadherin, and α-smooth muscle actin (α-SMA)), signal transducer (p-Smad2/3), and EMT initiator (Snail). ILK was also assayed by western blotting. The results showed that TGF-β1 induced spindle-like morphological transition in NRK-52E cells. Smad2/3 signaling pathway activation, increased fibronectin, α-SMA, ILK, and Snail expression, and decreased E-cadherin expression in TGF-β1-treated NRK-52E cells. FA efficiently blocked P-Smad2/3 activation and attenuated all these EMT changes induced by TGF-β1. These findings suggest that FA may serve as a potential fibrosis antagonist for renal proximal tubule cells by inhibiting EMT process. SN - 1741-427X UR - https://www.unboundmedicine.com/medline/citation/25949265/Ferulic_Acid_Attenuates_TGF_β1_Induced_Renal_Cellular_Fibrosis_in_NRK_52E_Cells_by_Inhibiting_Smad/ILK/Snail_Pathway_ L2 - https://doi.org/10.1155/2015/619720 DB - PRIME DP - Unbound Medicine ER -
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