Epigallocatechin-3-gallate (EGCG) has been recently proved to possess anti-inflammatory effects.

To investigate the effect and mechanism of epigallocatechin-3-gallate (EGCG) treatment in rats with acetic acid-induced colitis.

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-α (TNF-α) and interferon-γ (IFN-γ) and tissue expression of nuclear factor- Bp65 (NF- Bp65) were measured.

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±5.6μmol/gprot), MDA (0.9±0.6nmol/gprot), TNF-α (24.4±1.6PG/ml), IFN-γ (33.3±0.9PG/ml), and NF- Bp65 (28.0±2.8cells/mm³) 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).

EGCG exerts its antioxidant activity via decreasing NO, MDA, and increasing SOD. It ameliorates mucosal inflammation by inhibiting the production of TNF-α, IFN-γ and NF- Bp65 and may be a potential therapeutic agent in colitis.