title: 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.
abstract: 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.
authors.affiliation: Department of Internal Medicine, Chonnam National University Medical School, 8 Hak-Dong, Dong-ku, 501-757, Gwangju, Korea.
authors.forename: Young-A
authors.initials: YA
authors.lastname: Song
authors.forename: Young-Lan
authors.initials: YL
authors.lastname: Park
authors.forename: Sun-Hye
authors.initials: SH
authors.lastname: Yoon
authors.forename: Kyu-Yeol
authors.initials: KY
authors.lastname: Kim
authors.forename: Sung-Bum
authors.initials: SB
authors.lastname: Cho
authors.forename: Wan-Sik
authors.initials: WS
authors.lastname: Lee
authors.forename: Ik-Joo
authors.initials: IJ
authors.lastname: Chung
authors.forename: Young-Eun
authors.initials: YE
authors.lastname: Joo
mesh_terms: D000818:Animals; D044946:Biflavonoids / Q000494:pharmacology*; D002392:Catechin / Q000494:pharmacology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004847:Epithelial Cells / Q000378:metabolism*; D005419:Flavonoids / Q000737:chemistry*; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism*; D007422:Intestines / Q000166:cytology*; D008070:Lipopolysaccharides / Q000378:metabolism*; D048670:MAP Kinase Kinase 4 / Q000378:metabolism*; D020935:MAP Kinase Signaling System; D016328:NF-kappa B / Q000378:metabolism*; D010636:Phenols / Q000737:chemistry*; D059808:Polyphenols; D051381:Rats; D015398:Signal Transduction; D013662:Tea; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism*
chemical_list: D044946:Biflavonoids; D004791:Enzyme Inhibitors; D005419:Flavonoids; D008070:Lipopolysaccharides; D016328:NF-kappa B; D010636:Phenols; D059808:Polyphenols; D013662:Tea; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; C056068:theaflavin; D002392:Catechin; D048670:MAP Kinase Kinase 4