The Effect of (-)-Epigallocatechin-3-Gallate on IL-1β Induced IL-8 Expression in Orbital Fibroblast from Patients with Thyroid-Associated Ophthalmopathy.

Orbital fibroblasts have been reported to be an important effector cells for the development of thyroid-associated ophthalmopathy (TAO). Orbital fibroblasts secrete various inflammatory cytokines in response to an inflammatory stimulation, leading to TAO-related tissue swelling. It has also been rep...

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Main Authors: Ji-Young Lee, Ji-Sun Paik, Mihee Yun, Seong-Beom Lee, Suk-Woo Yang
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2016-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC4743944?pdf=render
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author Ji-Young Lee
Ji-Sun Paik
Mihee Yun
Seong-Beom Lee
Suk-Woo Yang
author_facet Ji-Young Lee
Ji-Sun Paik
Mihee Yun
Seong-Beom Lee
Suk-Woo Yang
author_sort Ji-Young Lee
collection DOAJ
description Orbital fibroblasts have been reported to be an important effector cells for the development of thyroid-associated ophthalmopathy (TAO). Orbital fibroblasts secrete various inflammatory cytokines in response to an inflammatory stimulation, leading to TAO-related tissue swelling. It has also been reported that (-)-epigallocatechin-3-gallate (EGCG), a major polyphenolic constituent of green tea, has antioxidant and anti-inflammatory properties. In the current study, we investigated the issue of whether or how EGCG affects the interleukin (IL)-1β-induced secretion of IL-8 in human orbital fibroblasts from TAO patients. Treatment with EGCG significantly reduced the level of IL-1β-induced secretion of IL-8 and the expression of IL-8 mRNA. IL-1β-induced the degradation of IκBα, and the phosphorylation of p38 and ERK, and the IL-1β-induced expression of IL-8 mRNA was inhibited by specific inhibitors, such as BAY-117085 for NF-kB, SB203580 for p38, and PD98059 for ERK. In addition, treatment with EGCG inhibited the IL-1β-induced degradation of IκBα, and the phosphorylation of p38 and ERK. However, pre-treatment with antioxidants, NVN and NAC, which suppressed ROS generation, did not reduce IL-8 expression in IL-1β-treated orbital fibroblasts, suggesting that the IL-1β-induced IL-8 expression is not mediated by the generation of ROS. These results show that EGCG suppresses the IL-1β-induced expression of IL-8 through inhibition of the NF-κB, p38, and ERK pathways. These findings could contribute to the development of new types of EGCG-containing pharmacological agents for use in the treatment of TAO.
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spelling doaj.art-e936043928254a82988925ed96c06e252022-12-22T03:35:23ZengPublic Library of Science (PLoS)PLoS ONE1932-62032016-01-01112e014864510.1371/journal.pone.0148645The Effect of (-)-Epigallocatechin-3-Gallate on IL-1β Induced IL-8 Expression in Orbital Fibroblast from Patients with Thyroid-Associated Ophthalmopathy.Ji-Young LeeJi-Sun PaikMihee YunSeong-Beom LeeSuk-Woo YangOrbital fibroblasts have been reported to be an important effector cells for the development of thyroid-associated ophthalmopathy (TAO). Orbital fibroblasts secrete various inflammatory cytokines in response to an inflammatory stimulation, leading to TAO-related tissue swelling. It has also been reported that (-)-epigallocatechin-3-gallate (EGCG), a major polyphenolic constituent of green tea, has antioxidant and anti-inflammatory properties. In the current study, we investigated the issue of whether or how EGCG affects the interleukin (IL)-1β-induced secretion of IL-8 in human orbital fibroblasts from TAO patients. Treatment with EGCG significantly reduced the level of IL-1β-induced secretion of IL-8 and the expression of IL-8 mRNA. IL-1β-induced the degradation of IκBα, and the phosphorylation of p38 and ERK, and the IL-1β-induced expression of IL-8 mRNA was inhibited by specific inhibitors, such as BAY-117085 for NF-kB, SB203580 for p38, and PD98059 for ERK. In addition, treatment with EGCG inhibited the IL-1β-induced degradation of IκBα, and the phosphorylation of p38 and ERK. However, pre-treatment with antioxidants, NVN and NAC, which suppressed ROS generation, did not reduce IL-8 expression in IL-1β-treated orbital fibroblasts, suggesting that the IL-1β-induced IL-8 expression is not mediated by the generation of ROS. These results show that EGCG suppresses the IL-1β-induced expression of IL-8 through inhibition of the NF-κB, p38, and ERK pathways. These findings could contribute to the development of new types of EGCG-containing pharmacological agents for use in the treatment of TAO.http://europepmc.org/articles/PMC4743944?pdf=render
spellingShingle Ji-Young Lee
Ji-Sun Paik
Mihee Yun
Seong-Beom Lee
Suk-Woo Yang
The Effect of (-)-Epigallocatechin-3-Gallate on IL-1β Induced IL-8 Expression in Orbital Fibroblast from Patients with Thyroid-Associated Ophthalmopathy.
PLoS ONE
title The Effect of (-)-Epigallocatechin-3-Gallate on IL-1β Induced IL-8 Expression in Orbital Fibroblast from Patients with Thyroid-Associated Ophthalmopathy.
title_full The Effect of (-)-Epigallocatechin-3-Gallate on IL-1β Induced IL-8 Expression in Orbital Fibroblast from Patients with Thyroid-Associated Ophthalmopathy.
title_fullStr The Effect of (-)-Epigallocatechin-3-Gallate on IL-1β Induced IL-8 Expression in Orbital Fibroblast from Patients with Thyroid-Associated Ophthalmopathy.
title_full_unstemmed The Effect of (-)-Epigallocatechin-3-Gallate on IL-1β Induced IL-8 Expression in Orbital Fibroblast from Patients with Thyroid-Associated Ophthalmopathy.
title_short The Effect of (-)-Epigallocatechin-3-Gallate on IL-1β Induced IL-8 Expression in Orbital Fibroblast from Patients with Thyroid-Associated Ophthalmopathy.
title_sort effect of epigallocatechin 3 gallate on il 1β induced il 8 expression in orbital fibroblast from patients with thyroid associated ophthalmopathy
url http://europepmc.org/articles/PMC4743944?pdf=render
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