(−)-Epigallocatechin gallate inhibits endotoxin-induced expression of inflammatory cytokines in human cerebral microvascular endothelial cells
<p>Abstract</p> <p>Background</p> <p>(−)-Epigallocatechin gallate (EGCG) is a major polyphenol component of green tea that has antioxidant activities. Lipopolysaccharide (LPS) induces inflammatory cytokine production and impairs blood–brain barrier (BBB) integrity. We e...
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Format: | Article |
Language: | English |
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BMC
2012-07-01
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Series: | Journal of Neuroinflammation |
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Online Access: | http://www.jneuroinflammation.com/content/9/1/161 |
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author | Li Jieliang Ye Li Wang Xu Liu Jinping Wang Yizhong Zhou Yu Ho Wenzhe |
author_facet | Li Jieliang Ye Li Wang Xu Liu Jinping Wang Yizhong Zhou Yu Ho Wenzhe |
author_sort | Li Jieliang |
collection | DOAJ |
description | <p>Abstract</p> <p>Background</p> <p>(−)-Epigallocatechin gallate (EGCG) is a major polyphenol component of green tea that has antioxidant activities. Lipopolysaccharide (LPS) induces inflammatory cytokine production and impairs blood–brain barrier (BBB) integrity. We examined the effect of EGCG on LPS-induced expression of the inflammatory cytokines in human cerebral microvascular endothelial cells (hCMECs) and BBB permeability.</p> <p>Methods</p> <p>The expression of TNF-α, IL-1β and monocyte chemotactic protein-1 (MCP-1/CCL2) was determined by quantitative real time PCR (qRT-PCR) and ELISA. Intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule (VCAM) in hCMECs were examined by qRT-PCR and Western blotting. Monocytes that adhered to LPS-stimulated endothelial cells were measured by monocyte adhesion assay. Tight junctional factors were detected by qRT-PCR (Claudin 5 and Occludin) and immunofluorescence staining (Claudin 5 and ZO-1). The permeability of the hCMEC monolayer was determined by fluorescence spectrophotometry of transmembrane fluorescin and transendothelial electrical resistance (TEER). NF-kB activation was measured by luciferase assay.</p> <p>Results</p> <p>EGCG significantly suppressed the LPS-induced expression of IL-1β and TNF-α in hCMECs. EGCG also inhibited the expression of MCP-1/CCL2, VCAM-1 and ICAM-1. Functional analysis showed that EGCG induced the expression of tight junction proteins (Occludin and Claudin-5) in hCMECs. Investigation of the mechanism showed that EGCG had the ability to inhibit LPS-mediated NF-κB activation. In addition, 67-kD laminin receptor was involved in the anti-inflammatory effect of EGCG.</p> <p>Conclusions</p> <p>Our results demonstrated that LPS induced inflammatory cytokine production in hCMECs, which could be attenuated by EGCG. These data indicate that EGCG has a therapeutic potential for endotoxin-mediated endothelial inflammation.</p> |
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issn | 1742-2094 |
language | English |
last_indexed | 2024-12-12T12:07:32Z |
publishDate | 2012-07-01 |
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series | Journal of Neuroinflammation |
spelling | doaj.art-af6a520984ea40719a0a394a74af981e2022-12-22T00:24:57ZengBMCJournal of Neuroinflammation1742-20942012-07-019116110.1186/1742-2094-9-161(−)-Epigallocatechin gallate inhibits endotoxin-induced expression of inflammatory cytokines in human cerebral microvascular endothelial cellsLi JieliangYe LiWang XuLiu JinpingWang YizhongZhou YuHo Wenzhe<p>Abstract</p> <p>Background</p> <p>(−)-Epigallocatechin gallate (EGCG) is a major polyphenol component of green tea that has antioxidant activities. Lipopolysaccharide (LPS) induces inflammatory cytokine production and impairs blood–brain barrier (BBB) integrity. We examined the effect of EGCG on LPS-induced expression of the inflammatory cytokines in human cerebral microvascular endothelial cells (hCMECs) and BBB permeability.</p> <p>Methods</p> <p>The expression of TNF-α, IL-1β and monocyte chemotactic protein-1 (MCP-1/CCL2) was determined by quantitative real time PCR (qRT-PCR) and ELISA. Intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule (VCAM) in hCMECs were examined by qRT-PCR and Western blotting. Monocytes that adhered to LPS-stimulated endothelial cells were measured by monocyte adhesion assay. Tight junctional factors were detected by qRT-PCR (Claudin 5 and Occludin) and immunofluorescence staining (Claudin 5 and ZO-1). The permeability of the hCMEC monolayer was determined by fluorescence spectrophotometry of transmembrane fluorescin and transendothelial electrical resistance (TEER). NF-kB activation was measured by luciferase assay.</p> <p>Results</p> <p>EGCG significantly suppressed the LPS-induced expression of IL-1β and TNF-α in hCMECs. EGCG also inhibited the expression of MCP-1/CCL2, VCAM-1 and ICAM-1. Functional analysis showed that EGCG induced the expression of tight junction proteins (Occludin and Claudin-5) in hCMECs. Investigation of the mechanism showed that EGCG had the ability to inhibit LPS-mediated NF-κB activation. In addition, 67-kD laminin receptor was involved in the anti-inflammatory effect of EGCG.</p> <p>Conclusions</p> <p>Our results demonstrated that LPS induced inflammatory cytokine production in hCMECs, which could be attenuated by EGCG. These data indicate that EGCG has a therapeutic potential for endotoxin-mediated endothelial inflammation.</p>http://www.jneuroinflammation.com/content/9/1/16167LRendothelial(−)-epigallocatechin gallateLPSNF-κB |
spellingShingle | Li Jieliang Ye Li Wang Xu Liu Jinping Wang Yizhong Zhou Yu Ho Wenzhe (−)-Epigallocatechin gallate inhibits endotoxin-induced expression of inflammatory cytokines in human cerebral microvascular endothelial cells Journal of Neuroinflammation 67LR endothelial (−)-epigallocatechin gallate LPS NF-κB |
title | (−)-Epigallocatechin gallate inhibits endotoxin-induced expression of inflammatory cytokines in human cerebral microvascular endothelial cells |
title_full | (−)-Epigallocatechin gallate inhibits endotoxin-induced expression of inflammatory cytokines in human cerebral microvascular endothelial cells |
title_fullStr | (−)-Epigallocatechin gallate inhibits endotoxin-induced expression of inflammatory cytokines in human cerebral microvascular endothelial cells |
title_full_unstemmed | (−)-Epigallocatechin gallate inhibits endotoxin-induced expression of inflammatory cytokines in human cerebral microvascular endothelial cells |
title_short | (−)-Epigallocatechin gallate inhibits endotoxin-induced expression of inflammatory cytokines in human cerebral microvascular endothelial cells |
title_sort | epigallocatechin gallate inhibits endotoxin induced expression of inflammatory cytokines in human cerebral microvascular endothelial cells |
topic | 67LR endothelial (−)-epigallocatechin gallate LPS NF-κB |
url | http://www.jneuroinflammation.com/content/9/1/161 |
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