Black tea polyphenol theaflavin suppresses LPS-induced ICAM-1 and VCAM-1 expression via blockage of NF-κB and JNK activation in intestinal epithelial cells.

OBJECTIVE: The aim of this study was to determine the impact of the black tea polyphenol, theaflavin, on the expression of adhesion molecules and activation of lipopolysaccharide (LPS)-induced innate signaling in rat intestinal epithelial (RIE) cells.
METHODS: The effect of theaflavin on neutrophil adhesion, expression of intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1, LPS-induced nuclear factor-kappa B (NF-κB), and mitogen-activated protein kinase (MAPK) signaling was examined by neutrophil adhesion assay, RT-PCR, Western blotting, immunofluorescence, and electrophoretic mobility shift assay (EMSA).
RESULTS: Theaflavin suppressed adhesion of neutrophils to LPS-stimulated RIE cells. LPS-induced ICAM-1 and VCAM-1 expressions were inhibited by theaflavin. LPS-induced IκBα phosphorylation/degradation and nuclear translocation of NF-κB/p65 were blocked by theaflavin. Also, theaflavin blocked NF-κB DNA-binding activity in EMSA. LPS-induced phosphorylation of JNK was inhibited by theaflavin. Bay11-7082 (a NF-κB inhibitor) and SP600125 (a JNK inhibitor) suppressed the LPS-induced ICAM-1 and VCAM-1 mRNA accumulations.
CONCLUSIONS: These results indicate that black tea polyphenol theaflavin suppresses LPS-induced ICAM-1 and VCAM-1 expressions through blockage of NF-κB and JNK activation in intestinal epithelial cells.