Reduction of oxidative stress and cytokine-induced neutrophil chemoattractant (CINC) expression by red wine polyphenols in zinc deficiency induced intestinal damage of rat.
Consumption of red wine has been associated with health promotion and disease prevention. We have previously found that the intestine of zinc-deficient (ZD) rats develop oxidative damage associated with inflammation. Here we have used this model to investigate whether red wine polyphenols could protect against intestinal injury and, if so, whether this protection was achieved through antioxidant and anti-inflammatory activity. The intestinal alterations induced by zinc deficiency such as morphological damage, increased TBA-RS level and CuZn-superoxide dismutase activity, and decreased glutathione peroxidase activity, did not develop with the administration to ZD rats of a suspension of dealcoholated red wine (RWS). The same treatment induced in control rats a decrease of TBA-RS level but also of glutathione peroxidase and catalase activity. Treatment with RWS to ZD rats prevented a marked mucosal macrophage and neutrophil infiltration. The expression of pro-inflammatory cytokines, such as tumor necrosis factor alpha and cytokine-induced neutrophil chemoattractant (CINC), was induced by zinc deficiency, whereas that of the anti-inflammatory interleukin-10 was suppressed. Treatment with RWS reduced CINC expression. These results report a novel activity of red wine polyphenols in downregulation of intestinal CINC expression, which likely protects cells against inflammatory processes.
Istituto Nazionale della Ricerca per gli Alimenti e la Nutrizione, Rome, Italy.
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Canali
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Vignolini
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Nobili
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Mengheri
D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000302:isolation & purification / Q000494:pharmacology; D000975:Antioxidants / Q000302:isolation & purification / Q000494:pharmacology; D001483:Base Sequence; D002374:Catalase / Q000378:metabolism; D019743:Chemokines, CXC; D002630:Chemotactic Factors / Q000235:genetics*; D017931:DNA Primers / Q000235:genetics; D005419:Flavonoids; D015870:Gene Expression / Q000187:drug effects; D005979:Glutathione Peroxidase / Q000378:metabolism; D006133:Growth Substances / Q000235:genetics*; D036341:Intercellular Signaling Peptides and Proteins; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000187:drug effects* / Q000293:injuries*; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects*; D009195:Peroxidase / Q000378:metabolism; D010636:Phenols / Q000302:isolation & purification / Q000494:pharmacology*; D011108:Polymers / Q000302:isolation & purification / Q000494:pharmacology*; D059808:Polyphenols; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics; D014920:Wine / Q000032:analysis*; D015032:Zinc / Q000172:deficiency
D000894:Anti-Inflammatory Agents, Non-Steroidal; D000975:Antioxidants; D019743:Chemokines, CXC; D002630:Chemotactic Factors; D017931:DNA Primers; D005419:Flavonoids; D006133:Growth Substances; D036341:Intercellular Signaling Peptides and Proteins; D010636:Phenols; D011108:Polymers; D059808:Polyphenols; D017392:Thiobarbituric Acid Reactive Substances; D014409:Tumor Necrosis Factor-alpha; D002374:Catalase; D009195:Peroxidase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D015032:Zinc