Epigallocatechin-3-gallate Inhibits LPS-Induced NF-kappaB and MAPK Signaling Pathways in Bone Marrow-Derived Macrophages
Gut and Liver
; : 188-196, 2012.
Article
en En
| WPRIM
| ID: wpr-19389
Biblioteca responsable:
WPRO
ABSTRACT
BACKGROUND/AIMS:
Epigallocatechin-3-gallate (EGCG), the primary catechin in green tea, has anti-inflammatory and anti-oxidative properties. The aim of the current study was to characterize the impact of EGCG on lipopolysaccharide (LPS)-induced innate signaling in bone marrow-derived macrophages (BMMs) isolated from ICR mice.METHODS:
The effect of EGCG on LPS-induced pro-inflammatory gene expression and nuclear factor-kappaB (NF-kappaB) and mitogen-activated protein kinase (MAPK) signaling was examined using reverse transcription-polymerase chain reaction, Western blotting, immunofluorescence, and the electrophoretic mobility shift assay.RESULTS:
EGCG inhibited accumulation of LPS-induced IL-12p40, IL-6, MCP-1, ICAM-1, and VCAM-1 mRNA in BMMs. EGCG blocked LPS-induced IkappaBalpha degradation and RelA nuclear translocation. EGCG blocked the DNA-binding activity of NF-kappaB. LPS-induced phosphorylation of ERK1/2, JNK, and p38 was inhibited by EGCG. U0126 (an inhibitor of MEK-1/2) suppressed the LPS-induced IL-12p40, IL-6, MCP-1, ICAM-1, and VCAM-1 mRNA accumulation in BMMs.CONCLUSIONS:
These results indicate that EGCG may prevent LPS-induced pro-inflammatory gene expression through blocking NF-kappaB and MAPK signaling pathways in BMMs.Palabras clave
Texto completo:
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Bases de datos:
WPRIM
Asunto principal:
Fosforilación
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Proteínas Quinasas
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Té
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Butadienos
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ARN Mensajero
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Catequina
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Expresión Génica
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Western Blotting
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FN-kappa B
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Técnica del Anticuerpo Fluorescente
Idioma:
En
Revista:
Gut and Liver
Año:
2012
Tipo del documento:
Article