Gut Liver.
2012 Apr;6(2):188-196.
Epigallocatechin-3-gallate Inhibits LPS-Induced NF-kappaB and MAPK Signaling Pathways in Bone Marrow-Derived Macrophages
- Affiliations
-
- 1Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea. yejoo@chonnam.ac.kr
- 2Department of Pharmacology, Chonnam National University Medical School, Gwangju, Korea.
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.