ScienceDirect® Home Skip Main Navigation Links
You have guest access to ScienceDirect. Find out more.
 
Home
Browse
My Settings
Alerts
Help
 Quick Search
 Search tips (Opens new window)
    Clear all fields    
advertisementadvertisement
European Journal of Pharmacology
Volume 579, Issues 1-3, 28 January 2008, Pages 411-417
 
Font Size: Decrease Font Size  Increase Font Size
 Abstract - selected
Article
Purchase PDF (959 K)

 
 
 
Related Articles in ScienceDirect
View More Related Articles
 
Special issue
View Record in Scopus
 
doi:10.1016/j.ejphar.2007.10.053    How to Cite or Link Using DOI (Opens New Window)
Copyright © 2007 Elsevier B.V. All rights reserved.

Therapeutic effect of epigallocatechin-3-gallate in a mouse model of colitis

Patricia A. Abbouda, Paul W. Hakea, Timothy J. Burroughsa, Kelli Odomsa, Michael O'Connora, Prajakta Mangeshkara, Hector R. Wonga and Basilia ZingarelliCorresponding Author Contact Information, a, E-mail The Corresponding Author

aCincinnati Children's Hospital Medical Center, Division of Critical Care Medicine, College of Medicine, University of Cincinnati, 3333 Burnet Avenue, Cincinnati, Ohio 45229, USA

Received 3 April 2007; 
revised 11 October 2007; 
accepted 16 October 2007. 
Available online 30 October 2007.

Purchase the full-text article



References and further reading may be available for this article. To view references and further reading you must purchase this article.

Abstract

Epigallocatechin-3-gallate (EGCG), a green tea catechin, has been shown to inhibit signaling pathways involved in inflammation, including nuclear factor-κB (NF-κB) and activator protein-1 (AP-1), which are important inducers of pro-inflammatory mediators. Aim of our study was to evaluate the therapeutic efficacy of EGCG in experimental colitis, which was induced by rectal administration of trinitrobenzenesulfonic acid (TNBS) in C57/BL6 mice. Mice were treated twice daily with vehicle or with EGCG (10 mg/kg) intraperitoneally, and sacrificed on days 1, 3, and 7 after TNBS administration. After induction of colitis, vehicle-treated mice experienced bloody diarrhea and loss of body weight. A remarkable colonic damage with hemorrhage, ulcers, and edema was observed and was associated with neutrophil infiltration as evaluated by myeloperoxidase (MPO) activity. Elevated plasma levels of tumor necrosis factor α, interleukin (IL)-6, IL-10 and keratinocyte-derived chemokine were also found. These events were paralleled by increased DNA binding of NF-κB and AP-1 in the colon of the vehicle-treated group. In contrast, the EGCG-treated mice experienced a very mild diarrhea and no weight loss. Damage of the colon was characterized by edema and hyperemia only. Tissue levels of MPO were also significantly reduced when compared to vehicle-treated mice. These beneficial effects of EGCG were associated with a significant reduction of NF-κB and AP-1 activation. However, treatment with EGCG did not reduce plasma cytokine levels. Our data demonstrate that EGCG may be beneficial in colitis through selective immunomodulatory effects, which may be mediated, at least in part, by inhibition of NF-κB and AP-1.

Keywords: Epigallocatechin-3-gallate; nuclear factor-κB; cytokines; neutrophils; colitis; activator-protein-1

Article Outline

1. Introduction
2. Materials and methods
2.1. Animals
2.2. Induction of colitis
2.3. Evaluation of colonic damage
2.4. Histopathological analysis
2.5. Determination of neutrophil infiltration
2.6. Plasma levels of cytokines
2.7. Nuclear protein extraction
2.8. Electrophoretic mobility shift assay
2.9. Materials
2.10. Data analysis
3. Results
3.1. Effect of EGCG on severity of colitis
3.2. Effect of EGCG on neutrophil infiltration in the colon
3.3. Effect of EGCG on plasma cytokine levels
3.4. EGCG inhibits NF-κB and AP-1 DNA binding
4. Discussion
References








 
Home
Browse
My Settings
Alerts
Help
Elsevier.com (Opens new window)
About ScienceDirect  |  Contact Us  |  Information for Advertisers  |  Terms & Conditions  |  Privacy Policy
Copyright © 2008 Elsevier B.V. All rights reserved. ScienceDirect® is a registered trademark of Elsevier B.V.