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Redox Biol. 2014 Jun 18;2:795-802. doi: 10.1016/j.redox.2014.06.008. eCollection 2014.

Wine consumption and intestinal redox homeostasis.

Author information

1
Department of Clinical and Biological Sciences, University of Turin at San Luigi Gonzaga Hospital, Orbassano, Turin 10043, Italy.
2
Department of Biomedical Sciences, University of Cagliari, Cagliari 09124, Italy.

Abstract

Regular consumption of moderate doses of wine is an integral part of the Mediterranean diet, which has long been considered to provide remarkable health benefits. Wine's beneficial effect has been attributed principally to its non-alcoholic portion, which has antioxidant properties, and contains a wide variety of phenolics, generally called polyphenols. Wine phenolics may prevent or delay the progression of intestinal diseases characterized by oxidative stress and inflammation, especially because they reach higher concentrations in the gut than in other tissues. They act as both free radical scavengers and modulators of specific inflammation-related genes involved in cellular redox signaling. In addition, the importance of wine polyphenols has recently been stressed for their ability to act as prebiotics and antimicrobial agents. Wine components have been proposed as an alternative natural approach to prevent or treat inflammatory bowel diseases. The difficulty remains to distinguish whether these positive properties are due only to polyphenols in wine or also to the alcohol intake, since many studies have reported ethanol to possess various beneficial effects. Our knowledge of the use of wine components in managing human intestinal inflammatory diseases is still quite limited, and further clinical studies may afford more solid evidence of their beneficial effects.

KEYWORDS:

AKT, serine/threonine protein kinase (v-akt murine thimoma viral oncogene homolog1); Antioxidants; CD, Crohns disease; COX-2, cyclooxygenase-2; Cys, cysteine; DSS, dextran sodium sulfate; ERK, extracellular signal-regulated kinase; GRP, grape reaction product; GSH, reduced glutathione; Gut; IBD, inflammatory bowel disease; IFN, interferon; IKB, inhibitor of NF-κB; IL, interleukin; Inflammation; LPS, lipopolysaccharide; MAPK, mitogen-activated protein kinase; NADPH, nicotinamide adenine dinucleotide phosphate reduced; NF-κB, nuclear factor-κB; Nrf2, nuclear factor erythroid-2-related factor 2; Oxidative stress; PGE-2, prostaglandin E-2; Polyphenols; ROS, reactive oxygen species; SIRT-1, silent mating type information regulation-1; TNF-α, tumor necrosis factor alpha; UC, Ulcerative Colitis; Wine; apoB48, apolipoprotein B48; iNOS, inducible nitric oxide synthase

PMID:
25009781
PMCID:
PMC4085343
DOI:
10.1016/j.redox.2014.06.008
[Indexed for MEDLINE]
Free PMC Article

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