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J Nutr Biochem. 2015 Jul;26(7):745-51. doi: 10.1016/j.jnutbio.2015.02.004. Epub 2015 Mar 27.

(-)-Epicatechin reduces blood pressure increase in high-fructose-fed rats: effects on the determinants of nitric oxide bioavailability.

Author information

1
Physical Chemistry-Institute for Molecular Biochemistry and Molecular Medicine (IBIMOL) School of Pharmacy and Biochemistry, University of Buenos Aires-National Council of Scientific and Technological Research (CONICET), Argentina.
2
Department of Pathology, School of Medicine, National University of Cuyo and Institute of Medicine and Experimental Biology-CONICET, Mendoza, Argentina.
3
Department of Biological Chemistry (IQUIFIB), School of Pharmacy and Biochemistry, University of Buenos Aires-National Council of Scientific and Technological Research (CONICET), Argentina.
4
Physiology-Institute of Drug Chemistry and Metabolism (IQUIMEFA), School of Pharmacy and Biochemistry, University of Buenos Aires-National Council of Scientific and Technological Research (CONICET), Argentina.
5
Department of Nutrition, University of California at Davis, Davis, CA 95616, USA; Department of Environmental Toxicology, University of California at Davis, Davis, CA 95616, USA.
6
Physical Chemistry-Institute for Molecular Biochemistry and Molecular Medicine (IBIMOL) School of Pharmacy and Biochemistry, University of Buenos Aires-National Council of Scientific and Technological Research (CONICET), Argentina. Electronic address: mgallean@ffyb.uba.ar.
7
Physical Chemistry-Institute for Molecular Biochemistry and Molecular Medicine (IBIMOL) School of Pharmacy and Biochemistry, University of Buenos Aires-National Council of Scientific and Technological Research (CONICET), Argentina; Department of Nutrition, University of California at Davis, Davis, CA 95616, USA.

Abstract

This work investigated the blood pressure (BP)-lowering effect of the flavanol (-)-epicatechin in a model of metabolic syndrome. Rats were fed a regular chow diet without (Control) or with 10% (w/v) fructose in the drinking water (high fructose, HF) for 8 weeks. A subgroup of the HF-fed rats was supplemented with (-)-epicatechin 20 mg/kg body weight (HF-EC). Dietary (-)-epicatechin reverted the increase in BP caused by the fructose treatment. In aorta, superoxide anion production and the expression of the NADPH oxidase (NOX) subunits p47(phox) and p22(phox) were enhanced in the HF-fed rats. The increase was prevented by (-)-epicatechin. Similar profile was observed for NOX4 expression. The activity of aorta nitric oxide synthase (NOS) was increased in the HF group and was even higher in the HF-EC rats. These effects were paralleled by increased endothelial NOS phosphorylation at the activation site Ser1177. Among the more relevant mitogen-activated protein kinase pathways in vascular tissue, c-Jun-N-terminal kinase was shown to be activated in the aorta of the HF-fed rats, and (-)-epicatechin supplementation mitigated this activation. Thus, the results suggest that dietary (-)-epicatechin supplementation prevented hypertension in HF-fed rats, decreasing superoxide anion production and elevating NOS activity, favoring an increase in NO bioavailability.

KEYWORDS:

Flavonoids; Fructose; Hypertension; Metabolic syndrome; Oxidants; Superoxide anion

PMID:
25943039
DOI:
10.1016/j.jnutbio.2015.02.004
[Indexed for MEDLINE]

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