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Randomized Controlled Trial
, 2015, 317348

Changes in LDL Oxidative Status and Oxidative and Inflammatory Gene Expression After Red Wine Intake in Healthy People: A Randomized Trial

Affiliations
Randomized Controlled Trial

Changes in LDL Oxidative Status and Oxidative and Inflammatory Gene Expression After Red Wine Intake in Healthy People: A Randomized Trial

Laura Di Renzo et al. Mediators Inflamm.

Abstract

Postprandial oxidative stress is characterized by an increased susceptibility of the organism towards oxidative damage after consumption of a meal rich in lipids and/or carbohydrates. Micronutrients modulate immune system and exert a protective action by reducing low density lipoproteins (LDL) oxidation via induction of antioxidant enzymes. We evaluated the gene expression of oxidative stress (HOSp), inflammasome (HIp), and human drug metabolism pathways (HDM) and ox-LDL level at baseline and after the intake of red wine naturally enriched with resveratrol (NPVRW), in association with or without a McDonald's meal (McDM). The ox-LDL levels significantly increase comparing baseline (B) versus McDM and decreased comparing McDM versus McDM + NPVRW (P ≤ 0.05). Percentages of significant genes expressed after each nutritional intervention were the following: (1) B versus McDM, 2.88% HOSp, 2.40% of HIp, and 3.37% of HDMp; (2) B versus McDM + NPVRW, 1.44% of HOSp, 4.81% of HIp, and 0.96% of HDMp; (3) McDM versus McDM + NPVRW, 2.40% of HOSp, 2.40% of HIp, and 5.77% of HDMp; (4) B versus NPVRW, 4.80% HOSp, 3.85% HIp, and 3.85% HDMp. NPVRW intake reduced postprandial ox-LDL and the expression of inflammation and oxidative stress related genes. Chronic studies on larger population are necessary before definitive conclusions.

Figures

Figure 1
Figure 1
Study design and intervention. The randomized crossover study was divided into 4 nutritional intervention treatments (T0, T1, T3, and T5). The collection of blood sample was detected to 3 hours to each intervention. Between every nutritional intervention, a wash-out period was inserted. In each treatment period subjects consumed (B) baseline (fasting); (C) McDonald's meal; (D) McDonald's meal with 250 mL of not pruned vineyard red wine; (E) 250 mL of not pruned vineyard red wine. Nutrition status was detected at step (A). The blood sample for nutrigenomic and biochemical analysis was collected at the end of each treatment period (T0, T2, T4, and T6).
Figure 2
Figure 2
Comparative values of ox-LDL level for each treatment intervention. The significant values are expressed as (a) baseline versus McDonald's meal (P ≤ 0.05); (b) McDonald's meal versus McDonald's meal + not pruned vineyard red wine (P ≤ 0.05); (c) baseline versus not pruned vineyard red wine (P > 0.05); baseline versus McDonald's meal + not pruned vineyard red wine (P > 0.05).
Figure 3
Figure 3
Expression of genomic pathways. Percentage of significant genes in comparison between: (a) baseline versus McDonald's meal; (b) baseline versus NPVRW; (c) baseline versus McDonald's meal + not pruned vineyard red wine; (d) McDonald's meal versus McDonald's meal + not pruned vineyard red wine.
Figure 4
Figure 4
Gene expression in each dietary intervention for inflammasome pathway. Different levels of up- and downregulation of genes analyzed between McDonald's meal andMcDonald's meal with not pruned vineyard red wine. The significant values are expressed as P ≤ 0.05 for a level of fold change >±2.00. Inflammasome genes: CASP8, Caspase 1 apoptosis related cysteine peptidase (NM_1228); CCL2, chemokine (C-C motif) Ligand 2 (NM_2982); IL6, Interleukin 6 (NM_600); NFKB1, Nuclear Factor of Kappa Light Polypeptides Gene Enhancer in B-Cells 1 (NM_3998).
Figure 5
Figure 5
Gene expression in each dietary intervention for oxidative stress pathway. Different levels of up- and downregulation of genes analyzed between McDonald's meal andMcDonald's meal with not pruned vineyard red wine. The significant values are expressed as P ≤ 0.05 for a level of fold change > ±2.00. Oxidative stress genes: CAT, Catalase (NM_1752); CCL5, Copper Chaperone for Superoxide Dismutase (NM_2985); GPX1, Glutathione Peroxidase 1 (NM_581); GPX2, Glutathione Peroxidase 1 (gastrointestinal) (NM_2083); SIRT2, Sirtuin 2 (NM_12237); SOD1, Superoxide Dismutase 1 Soluble (NM_454); TXN, Thioredoxin (NM_3329); UCP2, Uncoupling Protein 2 (Mitochondrial Proton Carrier) (NM_3355).
Figure 6
Figure 6
Gene expression in each dietary intervention for Human Drug Metabolism pathway. Different levels of up- and downregulation of genes analyzed between McDonald's meal andMcDonald's meal with not pruned vineyard red wine. The significant values are expressed as P ≤ 0.05 for a level of fold change ±2.00. Human Drug Metabolism genes: ADH4, Alcohol Dehydrogenase 4-Class 2 Pi Polypeptide (NM_670); ALDH1A1, Aldehyde Dehydrogenase 1 Family Member A1 (NM_689); ALOX5, Arachidonate 5-Lipoxygenase (NM_698); NAT1, N-Acetyltransferase 1 (Arylamine N-Acetyltransferase) (NM_662); NOS3, Nitric Oxide Synthase 3 (Endothelial Cell) (NM_603).
Figure 7
Figure 7
Nutrigenomic networking. Network showing upregulation (solid arrows) and downregulation (dashed arrows) of genes involved in inflammation, oxidative stress, and drug metabolism, in comparison with (a) baseline versus McD, (b) baseline versus NPVRW, (c) baseline versus McD + NPVRW, and (d) McD versus McD + NPVRW. Filled circle indicates upregulation in response to treatment; dashed circle indicates downregulation in response to treatment; empty circle indicates not significant genes. Oxidative stress genes: CAT, Catalase (NM_1752); GPX1, Glutathione Peroxidase 1 (NM_581); GPX2, Glutathione Peroxidase 1 (gastrointestinal) (NM_2083); UCP2, Uncoupling Protein 2 (Mitochondrial Proton Carrier) (NM_3355); SOD 1, Superoxide Dismutase 1 Soluble (NM_454); NOX4, Nadph. Oxidase 4 (NM_16931); ALB, Albumin (NM_477); CCL5, Copper Chaperone for Superoxide Dismutase (NM_2985). Inflammasome genes: CASP8, Caspase 1 Apoptosis Related Cysteine Peptidase (NM_1228); NFKB1, Nuclear Factor of Kappa Light Polypeptides Gene Enhancer in B-Cells 1 (NM_3998); CCL2, Chemokine (C-C motif) Ligand 2 (NM_2982); PYCARD, Pyd and Card Domain Containing (NM_13258); RPLP0, Ribosomal Protein Large P0 (NM_1002); NLRP12, Nrl Family Pyrin Domain Containing 12 (NM_33297); IL 6, Interleukin 6 (Interferon Beta 2) (NM_600). Human Drug Metabolism genes: NAT1, N-Acetyltransferase 1 (Arylamine N-Acetyltransferase) (NM_662); NOS3, Nitric Oxide Synthase 3 (Endothelial Cell) (NM_603); APOE, Apolipoprotein E (NM_41); ADH4, Alcohol Dehydrogenase 4-Class 2 Pi Polypeptide (NM_670); ALOX15, Arachidonate 15-Lipoxygenase (NM_1140); ALOX5, Arachidonate 5-Lipoxygenase (NM_698); HSD17 B2, Hydroxysteroid (17 Beta) Dehydrogenase 2 (NM_2153); ALDH1A1, Aldehyde Dehydrogenase 1 Family Member A1 (NM_689); MT2A, Metallothionein 2a (NM_5953).

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References

    1. Fan A., Wu X., Wu H., et al. Atheroprotective effect of oleoylethanolamide (OEA) targeting oxidized LDL. PLoS ONE. 2014;9(1):1–9. doi: 10.1371/journal.pone.0085337.e85337 - DOI - PMC - PubMed
    1. Maiolino G., Rossitto G., Caielli P., Bisogni V., Rossi G. P., Calò L. A. The role of oxidized low-density lipoproteins in atherosclerosis: the myths and the facts. Mediators of Inflammation. 2013;2013:13. doi: 10.1155/2013/714653.714653 - DOI - PMC - PubMed
    1. Alves M. I. B., Plaza F. A., Martínez-Tomás R., et al. Oxidized LDL and its correlation with lipid profile and oxidative stress biomarkers in young healthy Spanish subjects. Journal of Physiology and Biochemistry. 2010;66(3):221–227. doi: 10.1007/s13105-010-0028-4. - DOI - PubMed
    1. Iatbe H., Obama T., Kato R. The dynamics of oxidized LDL during atherogenesis. Journal Lipids. 2011;2011:9. doi: 10.1155/2011/418313.418313 - DOI - PMC - PubMed
    1. Zuliani G., Morieri M. L., Volpato S., et al. Determinants and clinical significance of plasma oxidized LDLs in older individuals. A 9 years follow-up study. Atherosclerosis. 2013;226(1):201–207. doi: 10.1016/j.atherosclerosis.2012.10.028. - DOI - PMC - PubMed

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