Epigallocatechin-3-gallate ameliorates rats colitis induced by acetic acid.
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.
Ran
Zhi Hua
ZH
Department of Gastroenterology, Shanghai Jiao Tong University, School of Medicine, Shanghai 200001, People's Republic of China. z-ran@online.sh.cn
Chen
Chi
C
Xiao
Shu Dong
SD
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
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