Epigallocatechin-3-gallate, constituent of green tea, suppresses the LPS-induced phenotypic and functional maturation of murine dendritic cells through inhibition of mitogen-activated protein kinases and NF-κB

被引:87
作者
Ahn, SC
Kim, GY
Kim, JH
Baik, SW
Han, MK
Lee, HJ
Moon, DO
Lee, CM
Kang, JH
Kim, BH
Oh, YH
Park, YM [1 ]
机构
[1] Pusan Natl Univ, Coll Med, Dept Microbiol, Pusan 602739, South Korea
[2] Pusan Natl Univ, Coll Nat Sci, Dept Microbiol, Pusan 609735, South Korea
[3] Pusan Natl Univ, Coll Med, Dept Anesthesia & Pain Med, Pusan 602739, South Korea
[4] Chonbuk Natl Univ, Sch Med, Dept Microbiol, Jeonju 560756, South Korea
[5] Inst Med Sci, Jeonju 560756, South Korea
[6] Dong A Univ, Coll Med, Med Res Ctr Canc Mol Therapy, Pusan 602723, South Korea
关键词
epigallocatechin-3-gallate; dendritic cell; mitogen-activated protein kinases; NF-kappa B;
D O I
10.1016/j.bbrc.2003.11.108
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The effects of epigallocatechin-3-gallate (EGCG) on dendritic cells (DC) maturation were investigated. EGCG, in a dose-dependent manner, profoundly inhibited CD80, CD86, and MHC class I and II expression on bone marrow-derived murine myeloid DC. EGCG restored the decreased dextran-FITC uptake and inhibited enhanced IL-12 production by LPS-treated DC. EGCG-treated DC were poor stimulators of naive allogeneic T-cell proliferation and reduced levels of IL-2 production in responding T cells. EGCG-pretreated DC inhibited LPS-induced MAPKs, such as ERK1/2, p38, JNK, and NF-kappaB p65 translocation. Therefore, the molecular mechanisms by which EGCG antagonized LPS-induced DC maturation appeared to involve the inhibition of MAPK and NF-kappaB activation. These novel findings provide new insight into the immunopharmacological role of EGCG and suggest a novel approach to the manipulation of DC for therapeutic application of autoimmune and allergic diseases. (C) 2003 Elsevier Inc. All rights reserved.
引用
收藏
页码:148 / 155
页数:8
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