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

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. 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-kappa B), and mitogen-activated protein kinase (MAPK) signaling was examined by neutrophil adhesion assay, RT-PCR, Western blotting, immunofluorescence, and electrophoretic mobility shift assay (EMSA). Theaflavin suppressed adhesion of neutrophils to LPS-stimulated RIE cells. LPS-induced ICAM-1 and VCAM-1 expressions were inhibited by theaflavin. LPS-induced I kappa B alpha phosphorylation/degradation and nuclear translocation of NF-kappa B/p65 were blocked by theaflavin. Also, theaflavin blocked NF-kappa B DNA-binding activity in EMSA. LPS-induced phosphorylation of JNK was inhibited by theaflavin. Bay11-7082 (a NF-kappa B inhibitor) and SP600125 (a JNK inhibitor) suppressed the LPS-induced ICAM-1 and VCAM-1 mRNA accumulations. These results indicate that black tea polyphenol theaflavin suppresses LPS-induced ICAM-1 and VCAM-1 expressions through blockage of NF-kappa B and JNK activation in intestinal epithelial cells.