Cocoa flavonoid epicatechin protects pancreatic beta cell viability and function against oxidative stress
Article first published online: 1 OCT 2013
© 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
Molecular Nutrition & Food Research
Volume 58, Issue 3, pages 447–456, March 2014
How to Cite
Martín, M. Á., Fernández-Millán, E., Ramos, S., Bravo, L. and Goya, L. (2014), Cocoa flavonoid epicatechin protects pancreatic beta cell viability and function against oxidative stress. Mol. Nutr. Food Res., 58: 447–456. doi: 10.1002/mnfr.201300291
- Issue published online: 4 MAR 2014
- Article first published online: 1 OCT 2013
- Manuscript Accepted: 25 JUL 2013
- Manuscript Revised: 23 JUL 2013
- Manuscript Received: 22 APR 2013
- Spanish Ministry of Economy and Competitivity. Grant Number: AGL2010–17579
- Antioxidant defenses;
- Cocoa flavanols;
- Dietary polyphenols;
- Oxidative biomarkers;
- Type 2 diabetes mellitus
Diabetes mellitus is associated with reductions in glutathione, supporting the critical role of oxidative stress in its pathogenesis. Antioxidant food components such as flavonoids have a protective role against oxidative stress-induced degenerative and age-related diseases. Flavonoids such as epicatechin (EC) constitute an important part of the human diet; they can be found in green tea, grapes, and cocoa and possess multiple biological activities. This study investigates the chemo-protective effect of EC against oxidative stress induced by tert-butylhydroperoxide (t-BOOH) on Ins-1E pancreatic beta cells.
Methods and results
Cell viability, oxidative status, phosphorylated Jun kinase (p-JNK) expression, and insulin secretion were evaluated. Ins-1E cells treatment with 5–20 μM EC for 20 h evoked no cell damage and enhanced antioxidant enzymes and insulin secretion. Addition of 50 μM t-BOOH for 2 h induced reactive oxygen species, p-JNK, and carbonyl groups and decreased GSH and insulin secretion. Pretreatment of cells with EC prevented the t-BOOH-induced reactive oxygen species, carbonyl groups, p-JNK expression and cell death, and recovered insulin secretion.
Ins-1E cells treated with EC showed a remarkable recovery of cell viability and insulin secretion damaged by t-BOOH, indicating that integrity of secreting and surviving machineries in the EC-treated cells was notably protected against the oxidative insult.