title: Epigallocatechin-3-gallate ameliorates rats colitis induced by acetic acid.
abstract: BACKGROUND
  Epigallocatechin-3-gallate (EGCG) has been recently proved to possess anti-inflammatory effects.
  
  
  OBJECTIVE
  To investigate the effect and mechanism of epigallocatechin-3-gallate (EGCG) treatment in rats with acetic acid-induced colitis.
  
  
  METHODS
  Sixty male rats were randomly assigned into 4 groups: normal control (n=10), model placebo (n=20), EGCG (n=15), and SASP (n=15). The normal group was treated with regular feeding, while the other 3 groups were treated orally with saline 2ml/d, EGCG 50mg/kg/d, and SASP 0.25g/kg/d, respectively, for 7 days using an established colitis model induced by 8% acetic acid. The disease activity index (DAI) and the therapeutic effects were evaluated. Colon mucosa damage index (CMDI) and histological score were determined. The activities of nitric oxide (NO), malondialdehyde (MDA), superoxide dismutase (SOD), tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) and tissue expression of nuclear factor-kappaBp65 (NF-kappaBp65) were measured.
  
  
  RESULTS
  EGCG notably improved the DAI (1.1+/-0.9), CMDI (1.5+/-0.9) and histological scores (4.6+/-3.1) compared with the placebo (3.9+/-0.4, p<0.01; 3.3+/-0.6, p<0.05; 9.3+/-2.8, p<0.01) and SASP groups (3.0+/-1.2, p<0.01; 2.3+/-0.9, p<0.05; 7.9+/-4.0, p<0.05). Compared with the placebo and SASP groups, the levels of NO (9.1+/-5.6micromol/gprot), MDA (0.9+/-0.6nmol/gprot), TNF-alpha (24.4+/-1.6PG/ml), IFN-gamma (33.3+/-0.9PG/ml), and NF-kappaBp65 (28.0+/-2.8cells/mm(3)) in EGCG-treated group were significantly reduced (p<0.05 or p<0.01), while that of SOD (185.4+/-24.6U/mgprot) was increased remarkably (p<0.05).
  
  
  CONCLUSIONS
  EGCG exerts its antioxidant activity via decreasing NO, MDA, and increasing SOD. It ameliorates mucosal inflammation by inhibiting the production of TNF-alpha, IFN-gamma and NF-kappaBp65 and may be a potential therapeutic agent in colitis.
authors.affiliation: Department of Gastroenterology, Shanghai Jiao Tong University, School of Medicine, Shanghai 200001, People's Republic of China. z-ran@online.sh.cn
authors.forename: Zhi Hua
authors.initials: ZH
authors.lastname: Ran
authors.forename: Chi
authors.initials: C
authors.lastname: Chen
authors.forename: Shu Dong
authors.initials: SD
authors.lastname: Xiao
mesh_terms: D019342:Acetic Acid; D000818:Animals; D002392:Catechin / Q000031:analogs & derivatives* / Q000494:pharmacology; D003092:Colitis / Q000139:chemically induced* / Q000188:drug therapy* / Q000473:pathology; D016207:Cytokines / Q000378:metabolism; D007202:Indicators and Reagents; D007371:Interferon-gamma / Q000378:metabolism; D007413:Intestinal Mucosa / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism; D051996:Transcription Factor RelA / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D016207:Cytokines; D007202:Indicators and Reagents; D051996:Transcription Factor RelA; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D008315:Malondialdehyde; D007371:Interferon-gamma; D002392:Catechin; C045651:epigallocatechin gallate; D013482:Superoxide Dismutase; D019342:Acetic Acid