Cocoa flavonoid epicatechin protects pancreatic beta cell viability and function against oxidative stress

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 a...

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Veröffentlicht in:Molecular nutrition & food research 2014-03, Vol.58 (3), p.447-456
Hauptverfasser: Martín, María Ángeles, Fernández‐Millán, Elisa, Ramos, Sonia, Bravo, Laura, Goya, Luis
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Sprache:eng
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Zusammenfassung: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‐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. CONCLUSION: 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.
ISSN:1613-4125
1613-4133
DOI:10.1002/mnfr.201300291