Cocoa flavonoids protect hepatic cells against high‐glucose‐induced oxidative stress: Relevance of MAPKs. Issue 4 (23rd February 2015)

• Record Type: Journal Article
• Authors: Cordero‐Herrera, Isabel; Martín, María Angeles; Goya, Luis; Ramos, Sonia
• Is Part Of: Molecular nutrition & food research. Volume 59:Issue 4(2015:Apr.)
• Page Start: 597
• Page End: 609
• Publication Date: 2015-02-23
• Subjects: Food -- Biotechnology -- Periodicals; Food -- Microbiology -- Periodicals; Nutrition -- Periodicals; Food -- Toxicology -- Periodicals; Nutrition -- Periodicals; Food Microbiology -- Periodicals; Food Technology -- Periodicals; Molecular Biology -- Periodicals; 664.0705
• DOI: 10.1002/mnfr.201400492
• Languages: English
• ISSNs: 1613-4125

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="mnfr2333-sec-0010" sec-type="section"> <title>Scope</title> <p>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.</p> </sec> <sec id="mnfr2333-sec-0020" sec-type="section"> <title>Methods and results</title> <p>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.</p> </sec> <sec id="mnfr2333-sec-0030" sec-type="section"> <title>Conclusion</title> <p>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.</p> </sec> </abstract>