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Effects of Epigallocatechin-3-Gallate on the Expression of TGF-β1, PKC α/βII, and NF-κB in High-Glucose-Stimulated Glomerular Epithelial Cells

Epigallocatechin-3-gallate (EGCG) is the most potent antioxidant polyphenol in green tea. In the present study, we investigated whether EGCG plays a role in the expression of transforming growth factor-beta1 (TGF-β1), protein kinase C (PKC) α/βII, and nuclear factor-kappaB (NF-κB) in glomerular epit...

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Autores principales: Park, Sung Jun, Jeong, Ji Min, Jeong, Han-Seong, Park, Jong-Seong, Kim, Nam-Ho
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Chonnam National University Medical School 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3214870/
https://www.ncbi.nlm.nih.gov/pubmed/22111071
http://dx.doi.org/10.4068/cmj.2011.47.2.116
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author Park, Sung Jun
Jeong, Ji Min
Jeong, Han-Seong
Park, Jong-Seong
Kim, Nam-Ho
author_facet Park, Sung Jun
Jeong, Ji Min
Jeong, Han-Seong
Park, Jong-Seong
Kim, Nam-Ho
author_sort Park, Sung Jun
collection PubMed
description Epigallocatechin-3-gallate (EGCG) is the most potent antioxidant polyphenol in green tea. In the present study, we investigated whether EGCG plays a role in the expression of transforming growth factor-beta1 (TGF-β1), protein kinase C (PKC) α/βII, and nuclear factor-kappaB (NF-κB) in glomerular epithelial cells (GECs) against high-glucose injury. Treatment with high glucose (30 mM) increased reactive oxygen species (ROS)/lipid peroxidation (LPO) and decreased glutathione (GSH) in GECs. Pretreatment with 100 µM EGCG attenuated the increase in ROS/LPO and restored the levels of GSH, whereas ROS, LPO, and GSH levels were not affected by treatment with 30 mM mannitol as an osmotic control. Interestingly, high-glucose treatment affected 3 separate signal transduction pathways in GECs. It increased the expression of TGF-β1, PKC α/βII, and NF-κB in GECs, respectively. EGCG (1, 10, 100 µM) pretreatment significantly decreased the expression of TGF-β1 induced by high glucose in a dose-dependent manner. In addition, EGCG (100 µM) inhibited the phosphorylation of PKC α/βII caused by glucose at 30 mM. Moreover, EGCG (1, 10, 100 µM) pretreatment significantly decreased the transcriptional activity of NF-κB induced by high glucose in a dose-dependent manner. These data suggest that EGCG could be a useful factor in modulating the injury to GECs caused by high glucose.
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spelling pubmed-32148702011-11-22 Effects of Epigallocatechin-3-Gallate on the Expression of TGF-β1, PKC α/βII, and NF-κB in High-Glucose-Stimulated Glomerular Epithelial Cells Park, Sung Jun Jeong, Ji Min Jeong, Han-Seong Park, Jong-Seong Kim, Nam-Ho Chonnam Med J Original Article Epigallocatechin-3-gallate (EGCG) is the most potent antioxidant polyphenol in green tea. In the present study, we investigated whether EGCG plays a role in the expression of transforming growth factor-beta1 (TGF-β1), protein kinase C (PKC) α/βII, and nuclear factor-kappaB (NF-κB) in glomerular epithelial cells (GECs) against high-glucose injury. Treatment with high glucose (30 mM) increased reactive oxygen species (ROS)/lipid peroxidation (LPO) and decreased glutathione (GSH) in GECs. Pretreatment with 100 µM EGCG attenuated the increase in ROS/LPO and restored the levels of GSH, whereas ROS, LPO, and GSH levels were not affected by treatment with 30 mM mannitol as an osmotic control. Interestingly, high-glucose treatment affected 3 separate signal transduction pathways in GECs. It increased the expression of TGF-β1, PKC α/βII, and NF-κB in GECs, respectively. EGCG (1, 10, 100 µM) pretreatment significantly decreased the expression of TGF-β1 induced by high glucose in a dose-dependent manner. In addition, EGCG (100 µM) inhibited the phosphorylation of PKC α/βII caused by glucose at 30 mM. Moreover, EGCG (1, 10, 100 µM) pretreatment significantly decreased the transcriptional activity of NF-κB induced by high glucose in a dose-dependent manner. These data suggest that EGCG could be a useful factor in modulating the injury to GECs caused by high glucose. Chonnam National University Medical School 2011-08 2011-08-31 /pmc/articles/PMC3214870/ /pubmed/22111071 http://dx.doi.org/10.4068/cmj.2011.47.2.116 Text en © Chonnam Medical Journal, 2011 http://creativecommons.org/licenses/by-nc/3.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Park, Sung Jun
Jeong, Ji Min
Jeong, Han-Seong
Park, Jong-Seong
Kim, Nam-Ho
Effects of Epigallocatechin-3-Gallate on the Expression of TGF-β1, PKC α/βII, and NF-κB in High-Glucose-Stimulated Glomerular Epithelial Cells
title Effects of Epigallocatechin-3-Gallate on the Expression of TGF-β1, PKC α/βII, and NF-κB in High-Glucose-Stimulated Glomerular Epithelial Cells
title_full Effects of Epigallocatechin-3-Gallate on the Expression of TGF-β1, PKC α/βII, and NF-κB in High-Glucose-Stimulated Glomerular Epithelial Cells
title_fullStr Effects of Epigallocatechin-3-Gallate on the Expression of TGF-β1, PKC α/βII, and NF-κB in High-Glucose-Stimulated Glomerular Epithelial Cells
title_full_unstemmed Effects of Epigallocatechin-3-Gallate on the Expression of TGF-β1, PKC α/βII, and NF-κB in High-Glucose-Stimulated Glomerular Epithelial Cells
title_short Effects of Epigallocatechin-3-Gallate on the Expression of TGF-β1, PKC α/βII, and NF-κB in High-Glucose-Stimulated Glomerular Epithelial Cells
title_sort effects of epigallocatechin-3-gallate on the expression of tgf-β1, pkc α/βii, and nf-κb in high-glucose-stimulated glomerular epithelial cells
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3214870/
https://www.ncbi.nlm.nih.gov/pubmed/22111071
http://dx.doi.org/10.4068/cmj.2011.47.2.116
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