Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea.
Gut Liver. 2012 Apr;6(2):188-96. doi: 10.5009/gnl.2012.6.2.188. Epub 2012 Apr 17.
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.
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.
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.
These results indicate that EGCG may prevent LPS-induced pro-inflammatory gene expression through blocking NF-κB and MAPK signaling pathways in BMMs.
背景/目的：表没食子儿茶素没食子酸酯（EGCG）是绿茶中的主要儿茶素，具有抗炎和抗氧化特性。本研究旨在探讨 EGCG 对 ICR 小鼠骨髓来源巨噬细胞（BMMs）中脂多糖（LPS）诱导的固有信号的影响。
采用逆转录-聚合酶链反应、Western blot、免疫荧光和电泳迁移率变动分析检测 EGCG 对 LPS 诱导的促炎基因表达和核因子-κB（NF-κB）和丝裂原活化蛋白激酶（MAPK）信号的影响。
EGCG 抑制 LPS 诱导的 BMMs 中 IL-12p40、IL-6、MCP-1、ICAM-1 和 VCAM-1mRNA 的积累。EGCG 阻断了 LPS 诱导的 IκBα降解和 RelA 核易位。EGCG 阻断了 NF-κB 的 DNA 结合活性。EGCG 抑制了 LPS 诱导的 ERK1/2、JNK 和 p38 的磷酸化。U0126（MEK-1/2 抑制剂）抑制了 LPS 诱导的 BMMs 中 IL-12p40、IL-6、MCP-1、ICAM-1 和 VCAM-1mRNA 的积累。
这些结果表明，EGCG 可能通过阻断 BMMs 中的 NF-κB 和 MAPK 信号通路来预防 LPS 诱导的促炎基因表达。
