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.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.