Epigallocatechin gallate, a constituent of green tea, suppresses cytokine-induced pancreatic beta-cell damage.
- Author:
Myung Kwan HAN
1
Author Information
1. Department of Life Science Division of Molecular and Life Science Pohang University of Science and Technology Pohang, Kyungbuk 790-784, Korea.
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
cytokine;
epigallocatechin gallate;
NF-kappaB;
nitric oxide
- MeSH:
Animals;
Blotting, Western;
Catechin/*analogs & derivatives/*pharmacology;
Cell Line;
Cell Survival/drug effects;
Cytokines/*antagonists & inhibitors/pharmacology;
Interferon Type II/antagonists & inhibitors/pharmacology;
Interleukin-1/antagonists & inhibitors/pharmacology;
Islets of Langerhans/cytology/*drug effects;
Nitric-Oxide Synthase/metabolism;
Nitrites/metabolism;
Tea/*chemistry
- From:Experimental & Molecular Medicine
2003;35(2):136-139
- CountryRepublic of Korea
- Language:English
-
Abstract:
Cytokines produced by immune cells infiltrating pancreatic islets have been implicated as one of the important mediators of beta-cell destruction in insulin-dependent diabetes mellitus. In this study, the protective effects of epigallocatechin gallate (EGCG) on cytokine-induced beta-cell destruction were investigated. EGCG effectively protected IL-1beta and IFN-g-mediated cytotoxicity in insulinoma cell line (RINm5F). EGCG induced a significant reduction in IL-1b and IFN-gamma-induced nitric oxide (NO) production and reduced levels of the inducible form of NO synthase (iNOS) mRNA and protein levels on RINm5F cells. The molecular mechanism by which EGCG inhibited iNOS gene expression appeared to involve the inhibition of NF-kB activation. These findings revealed EGCG as a possible therapeutic agent for the prevention of diabetes mellitus progression.
