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Cocoa flavonoid epicatechin protects pancreatic beta cell viability and function against oxidative stress
Author(s) -
Martín María Ángeles,
FernándezMillán Elisa,
Ramos Sonia,
Bravo Laura,
Goya Luis
Publication year - 2014
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201300291
Subject(s) - oxidative stress , viability assay , reactive oxygen species , antioxidant , glutathione , chemistry , insulin , secretion , oxidative phosphorylation , flavonoid , pharmacology , endocrinology , medicine , biochemistry , cell , biology , enzyme
Scope 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‐1 E pancreatic beta cells. Methods and results Cell viability, oxidative status, phosphorylated Jun kinase (p‐ JNK ) expression, and insulin secretion were evaluated. Ins‐1 E 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. Conclusion Ins‐1 E 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.