Epigallocatechin-3-gallate Reduces Mast Cells Activity TNF-α and NFKB in Colitis by Interrupting an Inflammatory Cascade (MUC2P.827)

Abstract

There is increasing evidence that (-)-epigallocatechin-3-gallate (EGCG) inhibits carcinogenesis and inflammation among other properties. However, its mechanism is not fully elucidated.To investigate the mechanism of action of EGCG in improving experimental colitis. 35 male Sprague-Dawley rats were randomly divided into 4 groups: Normal control group (n=5), EGCG group (n=9), TNBS group (n=9), and TNBS+EGCG group (n=12). For both, TNBS treated group and EGCG group, 1 mg/Kg EGCG was administered daily by intraperitoneal injection, starting one week before the induction. At days 3, 10 and 17, rats were sacrificed and the descending colon was collected. The score of histological alterations of the colonic mucosa was evaluated. The mast cells were assessed by toluidine blue staining. The mRNA expression of Tumor Necrosis Factor-α (TNF-α), and nuclear factor (NF-KB) was measured and ROS was tested by immunofluorescence. EGCG decreased significantly the erosions and the inflammatory cellular infiltration of the mucosa and submucosa. In addition, the mast cells were markedly reduced in number and degranulation. The increased levels NF-KB and TNF-α after TNBS administration were significantly and concurrently reduced in colonic scrapings after EGCG treatment at all the time points and did ROS. EGCG probably prevented the transcription of inflammatory genes by stabilizing mast cells and reducing its secretory pro-inflammatory factors such as TNF-α.