Epigallocatechin-3-gallate Inhibits the Expression of Adhesion Molecules by Blocking Nuclear Factor Kappa B Signaling in Intestinal Epithelial Cells

BACKGROUND/AIMS: Epigallocatechin-3-gallate (EGCG) is the main polyphenol in green tea and has anti-inflammatory and anti-oxidative effects. The aim of this study was to determine the impact of EGCG on the expression of adhesion molecules and lipopolysaccharide (LPS)-induced nuclear factor-kappa B (NF-kappaB) signaling in rat intestinal epithelial (RIE) cells. METHODS: The effect of EGCG on LPS-induced NF-kappaB signaling and expression of intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 was examined by reverse transcription polymerase chain reaction, western blotting, immunofluorescence and electrophoretic mobility shift assay. RESULTS: LPS-induced expression of ICAM-1 and VCAM-1 mRNA was inhibited by EGCG treatment in RIE cells. LPS-induced inhibitor of kappa B alpha degradation and NF-kappaB nuclear translocation were blocked by EGCG in RIE cells. EGCG blocked LPS-induced NF-kappaB DNA-binding activity in RIE cells. The pharmacological NF-kappaB inhibitor Bay11-7082 suppressed the LPS-induced expression of ICAM-1 and VCAM-1 mRNA in RIE cells. CONCLUSIONS: These results indicate that EGCG inhibits LPS-induced ICAM-1 and VCAM-1 expression by blocking NF-kappaB signaling in intestinal epithelial cells.

Epigallocatechin-3-gallate Inhibits LPS-Induced NF-kappaB and MAPK Signaling Pathways in Bone Marrow-Derived Macrophages

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.