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Poricoic acid A suppresses TGF-β1-induced renal fibrosis and proliferation via the PDGF-C, Smad3 and MAPK pathways

Renal interstitial fibrosis is the most important pathological process in chronic renal failure. Previous studies have shown that poricoic acid A (PAA), the main chemical constituent on the surface layer of the mushroom Poria cocos, has protective effects against oxidative stress and acute kidney in...

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Autores principales: Li, Qiang, Ming, Yao, Jia, Hu, Wang, Gang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7885072/
https://www.ncbi.nlm.nih.gov/pubmed/33717232
http://dx.doi.org/10.3892/etm.2021.9720
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author Li, Qiang
Ming, Yao
Jia, Hu
Wang, Gang
author_facet Li, Qiang
Ming, Yao
Jia, Hu
Wang, Gang
author_sort Li, Qiang
collection PubMed
description Renal interstitial fibrosis is the most important pathological process in chronic renal failure. Previous studies have shown that poricoic acid A (PAA), the main chemical constituent on the surface layer of the mushroom Poria cocos, has protective effects against oxidative stress and acute kidney injury. The present study aimed to investigate the potential roles of PAA on the pathological process of renal fibrosis and the associated molecular mechanism. The NRK-49F cell line was treated with transforming growth factor-β1 (TGF-β1) with or without PAA or platelet-derived growth factor C (PDGF-C). Cell Counting Kit-8 assay, western blotting and 5-ethynyl-2'-deoxyuridine immunofluorescence staining were performed to examine cell growth, protein expression and cell proliferation, respectively. Data from the present study showed that 10 µM PAA attenuated TGF-β1-induced NRK-49F cell extracellular matrix (ECM) accumulation, fibrosis formation and proliferation. Renal fibrosis with the activation of Smad3 and mitogen-activated protein kinase (MAPK) pathways were also inhibited by PAA treatment. PDGF-C reversed the inhibitory effects of PAA on TGF-β1-induced renal fibroblast proliferation and activation of the Smad3/MAPK pathway. The present study suggested that suppression of TGF-β1-induced renal fibroblast ECM accumulation, fibrosis formation and proliferation by PAA is mediated via the inhibition of the PDGF-C, Smad3 and MAPK pathways. The present findings not only revealed the potential anti-fibrotic effects of PAA on renal fibroblasts, but also provided a new insight into the prevention of fibrosis formation via regulation of the PDGF-C, Smad3 and MAPK signaling pathways.
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spelling pubmed-78850722021-03-12 Poricoic acid A suppresses TGF-β1-induced renal fibrosis and proliferation via the PDGF-C, Smad3 and MAPK pathways Li, Qiang Ming, Yao Jia, Hu Wang, Gang Exp Ther Med Articles Renal interstitial fibrosis is the most important pathological process in chronic renal failure. Previous studies have shown that poricoic acid A (PAA), the main chemical constituent on the surface layer of the mushroom Poria cocos, has protective effects against oxidative stress and acute kidney injury. The present study aimed to investigate the potential roles of PAA on the pathological process of renal fibrosis and the associated molecular mechanism. The NRK-49F cell line was treated with transforming growth factor-β1 (TGF-β1) with or without PAA or platelet-derived growth factor C (PDGF-C). Cell Counting Kit-8 assay, western blotting and 5-ethynyl-2'-deoxyuridine immunofluorescence staining were performed to examine cell growth, protein expression and cell proliferation, respectively. Data from the present study showed that 10 µM PAA attenuated TGF-β1-induced NRK-49F cell extracellular matrix (ECM) accumulation, fibrosis formation and proliferation. Renal fibrosis with the activation of Smad3 and mitogen-activated protein kinase (MAPK) pathways were also inhibited by PAA treatment. PDGF-C reversed the inhibitory effects of PAA on TGF-β1-induced renal fibroblast proliferation and activation of the Smad3/MAPK pathway. The present study suggested that suppression of TGF-β1-induced renal fibroblast ECM accumulation, fibrosis formation and proliferation by PAA is mediated via the inhibition of the PDGF-C, Smad3 and MAPK pathways. The present findings not only revealed the potential anti-fibrotic effects of PAA on renal fibroblasts, but also provided a new insight into the prevention of fibrosis formation via regulation of the PDGF-C, Smad3 and MAPK signaling pathways. D.A. Spandidos 2021-04 2021-01-27 /pmc/articles/PMC7885072/ /pubmed/33717232 http://dx.doi.org/10.3892/etm.2021.9720 Text en Copyright: © Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Li, Qiang
Ming, Yao
Jia, Hu
Wang, Gang
Poricoic acid A suppresses TGF-β1-induced renal fibrosis and proliferation via the PDGF-C, Smad3 and MAPK pathways
title Poricoic acid A suppresses TGF-β1-induced renal fibrosis and proliferation via the PDGF-C, Smad3 and MAPK pathways
title_full Poricoic acid A suppresses TGF-β1-induced renal fibrosis and proliferation via the PDGF-C, Smad3 and MAPK pathways
title_fullStr Poricoic acid A suppresses TGF-β1-induced renal fibrosis and proliferation via the PDGF-C, Smad3 and MAPK pathways
title_full_unstemmed Poricoic acid A suppresses TGF-β1-induced renal fibrosis and proliferation via the PDGF-C, Smad3 and MAPK pathways
title_short Poricoic acid A suppresses TGF-β1-induced renal fibrosis and proliferation via the PDGF-C, Smad3 and MAPK pathways
title_sort poricoic acid a suppresses tgf-β1-induced renal fibrosis and proliferation via the pdgf-c, smad3 and mapk pathways
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7885072/
https://www.ncbi.nlm.nih.gov/pubmed/33717232
http://dx.doi.org/10.3892/etm.2021.9720
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