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Intest Res. 2013 Oct;11(4):261-267. English. Original Article.
Myung DS , Park YL , Joo SY , Myung E , Chung CY , Park HC , Kim JS , Cho SB , Lee WS , Kim HS , Joo YE .
Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea.

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.

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