(-)-Epicatechin and the colonic metabolite 3,4-dihydroxyphenylacetic acid protect renal proximal tubular cell against high glucose-induced oxidative stress by modulating NOX-4/SIRT-1 signalling

被引:21
作者
Alvarez-Cilleros, David [1 ]
Angeles Martin, Maria [1 ,2 ]
Goya, Luis [1 ]
Ramos, Sonia [1 ]
机构
[1] CSIC, Inst Food Sci & Technol & Nutr ICTAN, Dept Metab & Nutr, Jose Antonio Novais 10,Ciudad Univ, Madrid 28040, Spain
[2] ISCIII, Ctr Invest Biomed Red Diabet & Enfermedades Metab, Madrid, Spain
关键词
Antioxidant defences; Colonic-derived flavonoid metabolites; Epicatechin; NRK-52E cells; Oxidative injury; Signalling pathways; NF-KAPPA-B; INFLAMMATORY RESPONSE; DIABETIC-NEPHROPATHY; COCOA POLYPHENOLS; ANTIOXIDANT; KIDNEY; EPICATECHIN; MECHANISMS; APOPTOSIS; ACETYLCYSTEINE;
D O I
10.1016/j.jff.2018.04.051
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
Oxidative stress plays a main role in the pathogenesis of the diabetic nephropathy. The present study investigated the effect of (-)-epicatechin (EC) and the colonic-derived flavonoid metabolites 2,3-dihydroxybenzoic acid, 3,4-dihydroxyphenylacetic acid (DHPAA), and 3-hydroxyphenylpropionic acid on the redox status in high-glucose-exposed renal proximal tubular NRK-52E cells. EC and DHPAA (10 mu M) alleviated the redox imbalance induced in high-glucose-challenged cells, as both compounds reverted to control levels reactive oxygen species (ROS) values. EC and DHPAA pre-treatment prevented the decrease of antioxidant defences and silent information regulator protein-1 (SIRT-1), and the increase of phosphorylated mitogen-activated-protein-kinases and NADPH-oxidase-4 (NOX-4) values under high-glucose-conditions. The presence of selective NOX-4 and SIRT-1 inhibitors in EC- and DHPAA-pre-treated cells showed the involvement of both proteins in EC- and DHPAA-mediated protection. These findings suggest that EC and DHPAA protected NRK-52E cells against a high-glucose-challenge by improving the cellular redox status through multiple signalling pathways, playing NOX-4/SIRT-1 a relevant role.
引用
收藏
页码:19 / 28
页数:10
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