Low dose Epigallocatechin Gallate Alleviates Experimental Colitis by Subduing Inflammatory Cells and Cytokines, and Improving Intestinal Permeability.
Animals
Anti-Inflammatory Agents
/ administration & dosage
Catechin
/ administration & dosage
Colitis
/ immunology
Colon
/ drug effects
Cytokines
/ immunology
Dextran Sulfate
Disease Models, Animal
Gastrointestinal Agents
/ administration & dosage
Inflammation Mediators
/ immunology
Macrophages
/ drug effects
Male
Mice, Inbred C57BL
Permeability
T-Lymphocytes
/ drug effects
animal model
epigallocatechin gallate (EGCG), cytokines
inflammatory bowel disease
Journal
Nutrients
ISSN: 2072-6643
Titre abrégé: Nutrients
Pays: Switzerland
ID NLM: 101521595
Informations de publication
Date de publication:
29 Jul 2019
29 Jul 2019
Historique:
received:
25
06
2019
revised:
10
07
2019
accepted:
26
07
2019
entrez:
1
8
2019
pubmed:
1
8
2019
medline:
21
1
2020
Statut:
epublish
Résumé
In this study, we investigate the impact of epigallocatechin gallate (EGCG), the most abundant and potent catechin in green tea, on a mouse model of inflammatory bowel disease (IBD) and the underlying mechanisms of action. C57BL/6J mice were subjected to dextran sulfate sodium (DSS)-induced IBD-like disease and then randomly divided into three groups: Model group (MD), low-dose EGCG group (LE, 20 mg/kg/d), and high-dose EGCG group (HE, 50 mg/kg/d). DSS-induced clinical and macroscopic changes were monitored daily. Intestinal permeability was assessed by FITC-Dextran assay. Both high- and low-dose EGCG treatment alleviated clinical manifestations including body weight loss and disease activity index (DAI) of DSS-induced colitis. The DAI score was significantly improved after two days of EGCG treatment. At the end of the study, the macroscopic severity score (MSS) of HE and LE treatment groups were 2.4 ± 1.2, and 2.2 ± 1.0, respectively, significantly lower than that of the controls (5.0 ± 2.1). EGCG treatment also prevented colon shortening, and improved intestinal permeability and histopathological changes. In addition, EGCG treatment attenuated colon inflammation by suppressing colonic levels of pro-inflammatory cytokines IL-6, MCP-1, and TNF-alpha, and inhibited CD3+ T cell and CD68+ macrophage infiltration. EGCG is effective in inflammatory colitis because it reduces cellular and molecular inflammation, and reduces intestinal permeability.
Sections du résumé
BACKGROUND
BACKGROUND
In this study, we investigate the impact of epigallocatechin gallate (EGCG), the most abundant and potent catechin in green tea, on a mouse model of inflammatory bowel disease (IBD) and the underlying mechanisms of action.
METHODS
METHODS
C57BL/6J mice were subjected to dextran sulfate sodium (DSS)-induced IBD-like disease and then randomly divided into three groups: Model group (MD), low-dose EGCG group (LE, 20 mg/kg/d), and high-dose EGCG group (HE, 50 mg/kg/d). DSS-induced clinical and macroscopic changes were monitored daily. Intestinal permeability was assessed by FITC-Dextran assay.
RESULTS
RESULTS
Both high- and low-dose EGCG treatment alleviated clinical manifestations including body weight loss and disease activity index (DAI) of DSS-induced colitis. The DAI score was significantly improved after two days of EGCG treatment. At the end of the study, the macroscopic severity score (MSS) of HE and LE treatment groups were 2.4 ± 1.2, and 2.2 ± 1.0, respectively, significantly lower than that of the controls (5.0 ± 2.1). EGCG treatment also prevented colon shortening, and improved intestinal permeability and histopathological changes. In addition, EGCG treatment attenuated colon inflammation by suppressing colonic levels of pro-inflammatory cytokines IL-6, MCP-1, and TNF-alpha, and inhibited CD3+ T cell and CD68+ macrophage infiltration.
CONCLUSION
CONCLUSIONS
EGCG is effective in inflammatory colitis because it reduces cellular and molecular inflammation, and reduces intestinal permeability.
Identifiants
pubmed: 31362373
pii: nu11081743
doi: 10.3390/nu11081743
pmc: PMC6724056
pii:
doi:
Substances chimiques
Anti-Inflammatory Agents
0
Cytokines
0
Gastrointestinal Agents
0
Inflammation Mediators
0
Catechin
8R1V1STN48
Dextran Sulfate
9042-14-2
epigallocatechin gallate
BQM438CTEL
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Déclaration de conflit d'intérêts
We have no conflict of interest to declare.
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