Epigallocatechin-3-gallate Inhibits the Expression of Adhesion Molecules by Blocking Nuclear Factor Kappa B Signaling in Intestinal Epithelial Cells.
- Author:
Dae Seong MYUNG
1
;
Young Lan PARK
;
So Young JOO
;
Eun MYUNG
;
Cho Yun CHUNG
;
Hyung Chul PARK
;
Jong Sun KIM
;
Sung Bum CHO
;
Wan Sik LEE
;
Hyun Soo KIM
;
Young Eun JOO
Author Information
- Publication Type:Original Article
- Keywords: Epigallocatechin gallate; Nuclear factor kappa B; Adhesion molecule; Intestinal epithelial cell
- MeSH: Animals; Blotting, Western; Catechin; Epithelial Cells*; Fluorescent Antibody Technique; Intercellular Adhesion Molecule-1; NF-kappa B*; Nitriles; Polymerase Chain Reaction; Rats; Reverse Transcription; RNA, Messenger; Sulfones; Tea; Vascular Cell Adhesion Molecule-1
- From:Intestinal Research 2013;11(4):261-267
- CountryRepublic of Korea
- Language:English
- Abstract: 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.
