Objective: To explore the protective effect of epigallocatechin-3-gallate (EGCG) on ulcerative colitis (UC) and mechanism thereof.
Methods: Sixty SD rats underwent enema of trinitrobenzene sulfonic acid (TNBS) to cause UC and then randomly divided into 6 groups: model group, undergoing enema of normal saline (NS) once a day for 2 weeks; positive drug control group, undergoing enema of 5-aminosalicylic acid (ASA), an anti-UC drug; high-dose EGCG group, undergoing enema of 100 mg/kg EGCG; low-dose EGCG group, undergoing 5 enema of 50 mg/kg EGCG; and EGCG pretreatment group, undergoing enema of 100 mg/kg once a day 3 days before the model establishment and then once a day for 2 weeks after the model establishment. Another 12 rats were used as normal controls. Two weeks later the rats were killed. The histological score of the colonic mucosa was evaluated. The cyclooxygenase-2 protein expression in the colonic mucosa was detected by immunohistochemistry and the cyclooxygenase-2 mRNA expression was assessed by semiquantitative reverse-transcription polymerase chain reaction.
Results: The histological score of the model group was 6.4 +/- 2.7, significantly higher than that of the normal control group (1.0 +/- 0.7, P < 0.01). The histological scores of the 5-ASA, and 100 mg/kg and 50 mg/kg EGCG groups were 3.4 +/- 1.8, 2.6 +/- 1.5, and 4.0 +/- 2.0 respectively, all significantly lower than that of the model group (all P < 0.05). The histological scores of the EGCG pretreatment group was the lowest (1.2 +/- 0.8), especially compared with the model group (P < 0.01). Cyclooxygenase -2 mRNA was not expressed in the normal control group, was highly expressed in the model group, and the expression levels of the 5-ASA and EGCG groups were all significantly lower than that of the model group (chi(2) = 22.017, P < 0.05).
Conclusion: Preventing and ameliorating colitis by inhibiting cyclooxygenase-2 activity, EGCG may be a potential medicine in treating inflammatory bowel disease.