title: Black tea extract prevents lipopolysaccharide-induced NF-κB signaling and attenuates dextran sulfate sodium-induced experimental colitis.
abstract: BACKGROUND
  Black tea has been shown to elicit anti-oxidant, anti-carcinogenic, anti-inflammatory and anti-mutagenic properties. In this study, we investigated the impact of black tea extract (BTE) on lipopolysaccharide (LPS)-induced NF-κB signaling in bone marrow derived-macrophages (BMM) and determined the therapeutic efficacy of this extract on colon inflammation.
  
  
  METHODS
  The effect of BTE on LPS-induced NF-κB signaling and pro-inflammatory gene expression was evaluated by RT-PCR, Western blotting, immunofluorescence and electrophoretic mobility shift assay (EMSA). The in vivo efficacy of BTE was assessed in mice with 3% dextran sulfate sodium (DSS)-induced colitis. The severity of colitis was measured by weight loss, colon length and histologic scores.
  
  
  RESULTS
  LPS-induced IL-12p40, IL-23p19, IL-6 and IL-1β mRNA expressions were inhibited by BTE. LPS-induced IκBα phosphorylation/degradation and nuclear translocation of NF-κB/p65 were blocked by BTE. BTE treatment blocked LPS-induced DNA-binding activity of NF-κB. BTE-fed, DSS-exposed mice showed the less weight loss, longer colon length and lower histologic score compared to control diet-fed, DSS-exposed mice. DSS-induced IκBα phosphorylation/degradation and phosphorylation of NF-κB/p65 were blocked by BTE. An increase of cleaved caspase-3 and poly (ADP-ribose) polymerase (PARP) in DSS-exposed mice was blocked by BTE.
  
  
  CONCLUSIONS
  These results indicate that BTE attenuates colon inflammation through the blockage of NF-κB signaling and apoptosis in DSS-induced experimental colitis model.
authors: Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea.
authors: Young-A
authors: YA
authors: Song
authors: Young-Lan
authors: YL
authors: Park
authors: Kyu-Yeol
authors: KY
authors: Kim
authors: Cho-Yun
authors: CY
authors: Chung
authors: Gi-Hoon
authors: GH
authors: Lee
authors: Dae-Ho
authors: DH
authors: Cho
authors: Ho-Seok
authors: HS
authors: Ki
authors: Kang-Jin
authors: KJ
authors: Park
authors: Sung-Bum
authors: SB
authors: Cho
authors: Wan-Sik
authors: WS
authors: Lee
authors: Nacksung
authors: N
authors: Kim
authors: Bong-Whan
authors: BW
authors: Ahn
authors: Young-Eun
authors: YE
authors: Joo
mesh_terms: D000818:Animals; D028241:Camellia sinensis / Q000737:chemistry*; D002478:Cells, Cultured; D003092:Colitis / Q000139:chemically induced / Q000188:drug therapy* / Q000235:genetics / Q000276:immunology; D016207:Cytokines / Q000235:genetics / Q000276:immunology; D016264:Dextran Sulfate / Q000009:adverse effects; D004195:Disease Models, Animal; D015536:Down-Regulation / Q000187:drug effects*; D015870:Gene Expression / Q000187:drug effects; D006801:Humans; D008070:Lipopolysaccharides / Q000276:immunology*; D008264:Macrophages / Q000187:drug effects / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D016328:NF-kappa B / Q000276:immunology*; D010936:Plant Extracts / Q000494:pharmacology*; D015398:Signal Transduction / Q000187:drug effects*
chemical_list: D016207:Cytokines; D008070:Lipopolysaccharides; D016328:NF-kappa B; D010936:Plant Extracts; D016264:Dextran Sulfate