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Cocoa flavonoids protect hepatic cells against high‐glucose‐induced oxidative stress: Relevance of MAPKs
Author(s) -
CorderoHerrera Isabel,
Martín María Angeles,
Goya Luis,
Ramos Sonia
Publication year - 2015
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.201400492
Subject(s) - oxidative stress , insulin resistance , oxidative phosphorylation , antioxidant , chemistry , kinase , insulin , pharmacology , mapk/erk pathway , glucose uptake , biochemistry , medicine , endocrinology , biology
Scope Oxidative stress plays a main role in the pathogenesis of type 2 diabetes mellitus. Cocoa and (‐)‐epicatechin (EC), a main cocoa flavanol, have been suggested to exert beneficial effects in type 2 diabetes mellitus because of their protective effects against oxidative stress and insulin‐like properties. In this study, the protective effect of EC and a cocoa phenolic extract (CPE) against oxidative stress induced by a high‐glucose challenge, which causes insulin resistance, was investigated on hepatic HepG2 cells. Methods and results Oxidative status, phosphorylated mitogen‐activated protein kinases (MAPKs), nuclear factor E2 related factor 2 (Nrf2) and p‐(Ser)‐IRS‐1 expression, and glucose uptake were evaluated. EC and CPE regulated antioxidant enzymes and activated extracellular‐regulated kinase and Nrf2. EC and CPE pre‐treatment prevented high‐glucose‐induced antioxidant defences and p‐MAPKs, and maintained Nrf2 stimulation. The presence of selective MAPK inhibitors induced changes in redox status, glucose uptake, p‐(Ser)‐ and total IRS‐1 levels that were observed in CPE‐mediated protection. Conclusion EC and CPE recovered redox status of insulin‐resistant HepG2 cells, suggesting that the functionality in EC‐ and CPE‐treated cells was protected against high‐glucose‐induced oxidative insult. CPE beneficial effects on redox balance and insulin resistance were mediated by targeting MAPKs.