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-gamma-mediated cytotoxicity in insulinoma cell line (RINm5F). EGCG induced a significant reduction in IL-1beta 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-kappaB activation. These findings revealed EGCG as a possible therapeutic agent for the prevention of diabetes mellitus progression.
Highlights
Epigallocatechin gallate (EGCG), a major ingredient of green tea has been known to have a variety of physiological activities; anticarcinogenic, antioxidant, antiangiogenic, and antiviral activity (Nakayama et al, 1993; Yang and Wang, 1993; Katiyar and Mukhtar, 1997)
Mediation by cytokines secreted by the infiltrating immune cells was reported to illicit cytotoxicity of pancreatic β-cell is mediated by cytokines (Rabinovitch and Suarez-Pinzon, 1998; Tannous et al, 2001)
These results suggest that cytokine-induced up-regulation of inducible form of nitric oxide (NO) synthase (iNOS) in pancreatic β-cell may contribute in generation of Insulin-dependent diabetes mellitus (IDDM), and intervention of iNOS-induction could provide an effective means to prevent or treat onset of the disease
Summary
Epigallocatechin gallate (EGCG), a major ingredient of green tea has been known to have a variety of physiological activities; anticarcinogenic, antioxidant, antiangiogenic, and antiviral activity (Nakayama et al, 1993; Yang and Wang, 1993; Katiyar and Mukhtar, 1997). Tannous et al (Tannous et al, 2001) have demonstrated that cytokine-induced pancreatic β-cell damage is primarily associated with the induction of inducible nitric oxide synthase (iNOS), leading to the generation of nitric oxide (NO) within the cell, which subsequently causes dysfuction of the pancreatic βcell. Together, these results suggest that cytokine-induced up-regulation of iNOS in pancreatic β-cell may contribute in generation of IDDM, and intervention of iNOS-induction could provide an effective means to prevent or treat onset of the disease. We show that EGCG protected cytokine-induced β-cell damage, which is partly mediated by suppression of NF-κB or iNOS activity
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