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KMID : 1188320120060020188
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Gut and Liver
2012 Volume.6 No. 2 p.188 ~ p.196
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Epigallocatechin-3-gallate Inhibits LPS-Induced NF-κB and MAPK Signaling Pathways in Bone Marrow-Derived Macrophages
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Joo So-Young
Song Young-A
Park Young-Lan
Myung Eun
Chung Cho-Yun
Park Kang-Jin
Cho Sung-Bum
Lee Wan-Sik
Kim Hyun-Soo
Rew Jong-Sun
Kim Nack-Sung
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Abstract
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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-κB (NF-κB) 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 IκBα degradation and RelA nuclear translocation. EGCG blocked the DNA-binding activity of NF-κB. 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-κB and MAPK signaling pathways in BMMs.
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KEYWORD
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Epigallocatechin-3-gallate, Nuclear factor-κB, Mitogen-activated protein kinase, Macrophage
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