961 resultados para matrix metalloproteinase 2
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Rsumant mon travail de thse, l'article qui suit dcrit un nouveau modle animal servant tudier l'impact combin d'une ventilation mcanique (VM), d'une oxygnothrapie et d'une inflammation sur des poumons immatures. Cette tude permet, pour la premire fois, de mesurer l'expression de gnes distance d'une VM pour en analyser la cintique. La VM reprsente un traitement intgral dans la prise en charge de prmaturs. Sauvant des vies, elle est cependant non-physiologique et dcrite comme nocive court et long terme, empchant le bon dveloppement pulmonaire. Nombreuses tudes se sont intresses l'impact immdiat de la VM sur les poumons, mais il n'existe ce jour aucun modle de rongeur pour en analyser les effets tardifs. Par analogie avec la clinique, nous avons cr un modle avec un animal dont le stade dveloppemental pulmonaire est comparable aux prmaturs humains et consistant en une oxygnothrapie, une VM modre avec intubation non chirurgicale, similaire la pratique quotidienne, et un contexte inflammatoire mimant celui de chorioamnionite dans lequel bien des prmaturs naissent. Nous avons ensuite ralis une extubation pour permettre une priode de rtablissement, puis fait des analyses et sur le plan structurel par histologie conventionnelle et en 3D, et sur le plan biologique, par analyse de l'expression de gnes et de protines. Ce travail a permis de valider ce nouveau modle comme outil de recherche pour raliser des mesures distance d'une VM chez des rats nouveau-ns. Comparant ces mesures celles prises la fin de la VM, nous observons: une augmentation initiale et transitoire des mdiateurs impliqus dans la cascade inflammatoire dont le corrlat histologique est une maladie inflammatoire pulmonaire et, tardivement, une altration plus dveloppementale de la structure pulmonaire avec diminution de l'alvolarisation. Ceci pourrait tre en partie d une expression asynchrone de gnes dcrits comme importants pour la formation des alvoles (matrix metalloproteinase 9, elastine). Offrant une nouvelle approche pour la recherche pulmonaire chez les rongeurs, ce modle servira comme futur outil pour approfondir nos connaissances de la physiopathologie conduisant aux altrations structurelles retrouves dans les poumons d'anciens prmaturs soumis une VM (dysplasie broncho-pulmonaire), pour tester l'influence de certains traitements (p.ex. surfactant) et pour tudier les effets de la VM en l'appliquant des modles transgniques.
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The present experiment describes an easy procedure for obtaining SiO2/ZrO2 by reacting ZrOCl2 with SiO2 with the following characteristics: S BET = 500 m g-1 and an average pore diameter of 6 nm. The material obtained presented 1.3 wt% ZrO2 content corresponding to 140 mumol g-1. The average density of ZrO2 onto SiO2/ZrO2 matrix is 2.8x10-11 mol cm-2. The adsorption isotherm for Cr(VI) showed a maximum of adsorption value (200 mumol g-1) at pH 2. The adsorption can be described by the reaction: =Zr(OH)2 + 2HCrO4- + 2H+ <IMG SRC="http:/img/fbpe/qn/v25n3/9346fr1.gif">[(=Zr(OH2+)2) (HCrO4-)2]. Above the zero point of charge, i.e. pH > 5.5 due to the surface charge inversion, desorption of Cr(VI) occurs according to the reaction: [(=Zr(OH2+)2) (HCrO4-)2] + 6OH- <IMG SRC="http:/img/fbpe/qn/v25n3/9346fr1.gif">(=ZrO2)2- + 6H2O + 2CrO4(2-).
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Salivary gland cancer (SGC) is a rare cancer. The histological classification of SGC is complex and its biological behavior highly variable: it may vary from a low-grade tumor to a high-grade and often fatal malignancy. These circumstances make this cancer a diagnostic and therapeutic challenge. Older age and exposure to ionizing radiation are known risk factors. The mainstay of treatment is surgery combined with adjuvant radiation therapy, when appropriate. In addition to the histological type, the only well known prognostic factor is the TNM classification, which describes the tumor size and the amount of metastases. This study was performed using a full population-based nationwide cohort of SGC patients and tumors diagnosed in Finland in 1991-1996. The annual incidence of SGC in the entire population was, on average, 47.7 per year. By histological re-evaluation of 237 specimens the most frequent histological types were the adenoid cystic carcinoma (n=65; 27%), the mucoepidermoid carcinoma (n=45; 19%) and the acinic cell carcinoma (n=41; 17%). The highest 10-year disease-specific survival rate occurred among patients with acinic cell carcinoma (90%), followed by mucoepidermoid carcinoma (81%) and adenoid cystic carcinoma (60%). A high volume-corrected index (VCI) of Ki-67 correlated with worse survival of patients with SGC. Computer-assisted morphometric analyses of CD34-positive vessels indicated an unfavorable prognosis for patients with mucoepidermoid carcinoma and an association with poor survival among patients with acinic cell carcinoma. A high level of expression of matrix metalloproteinase-9 (MMP-9) showed a trend for a poorer prognosis in salivary duct carcinoma, and a high level of MMP-13 and a low level of MMP-1 had a trend for a poorer prognosis of patients with SGC. A low level of MMP-7 was associated with a poor prognosis of patients with acinic cell and mucoepidermoid carcinoma.
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Different common drugs (Meloxicam, Tenoxicam and Piroxicam, and sodium alendronate) were tested both experimental and theoretically as inhibitors of interstitial human collagenase, also known as matrix metalloproteinase 1 (MMP-1). The in vitro collagenase activity, alone and in the presence of inhibitors, was quantified by the reaction with a fluorescent synthetic substrate and measuring the change of emission. Collagenase-inhibitor interaction was studied theoretically by computational calculations. Three among the four tested substances showed moderate inhibiting activity against the human collagenase.
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<b>Studies on <sup>68</sup>Ga-Based Agents for PET Imaging of Cancer and Inflammation</b> Positron emission tomography (PET) is based on the use of radiolabeled agents and facilitates in vivo imaging of biological processes, such as cancer. Because the detection of cancer is demanding and is often obscured by inflammation, there is a demand for better PET imaging agents. The aim was to preliminarily evaluate new PET agents for imaging cancer and inflammation using experimental models. <sup>68</sup>Ga-chloride and peptides, <sup>68</sup>Ga-labeled through 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetraacetic acid (DOTA), targeting matrix metalloproteinase-9 (MMP-9) were tested for tumor imaging. In addition, a <sup>68</sup>Ga-DOTA-conjugated peptide targeting vascular adhesion protein-1 (VAP-1), was tested for inflammation imaging. The <sup>68</sup>Ga-based imaging agents described here showed potential features by passing the essential <i>in vitro</i> tests, proceeding further to preclinical <i>in vivo</i> evaluation and being able to visualize the target. The target uptake and target-to-background ratios of <sup>68</sup>Ga-based agents were, however, not optimal. <sup>68</sup>Ga-chloride showed slow clearance caused by its binding to blood transferrin. In the case of <sup>68</sup>Ga-DOTA-peptides low <i>in vivo</i> stability and/or low lipophilicity led to too rapid blood clearance and urinary excretion. The properties of <sup>68</sup>Ga-labeled peptides are modifiable, as shown with matrix metalloproteinase-9 targeting ligands. In the conclusion of this PhD thesis, <sup>68</sup>Ga-based agents for PET imaging of cancer and inflammation could be applied in the development of drugs, earlier diagnostics and following-up of the efficacy of therapies.
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Matrix metalloproteinase-13 (MMP-13) is a potent proteolytic enzyme, whose expression has been previously associated with fetal bone development and postnatal bone remodeling and with adult gingival wound healing. MMP-13 is also known to be involved in the growth and invasion of various cancers including squamous cell carcinoma (SCC) of the skin. The aim of this study was to further elucidate the function and regulation of MMP-13 in wound repair and cancer. In this study, it was shown that fetal skin fibroblasts express MMP-13 in response to transforming growth factor- in a p38 MAP kinase dependent manner. In addition, MMP-13 was found to be expressed in vivo by wound fibroblasts in human fetal skin grafted on SCID mice. Adenovirally delivered expression of MMP-13 enhanced collagen matrix contraction by fibroblasts in vitro in association with altered cytoskeletal structure, enhanced proliferation and survival. These results indicate that MMP-13 is involved in cell-mediated collagen matrix remodeling and suggest a role for MMP-13 in superior matrix remodeling and scarless healing of fetal skin wounds. Using an MMP-13 deficient mouse strain, it was shown that MMP-13 is essential for the normal development of experimental granulation tissue in mice. MMP-13 was implicated in the regulation of myofibroblast function and angiogenesis and the expression of genes involved in cellular proliferation and movement, immune response, angiogenesis and proteolysis. Finally, epidermal mitogen, keratinocyte growth factor (KGF) was shown to suppress the malignant properties of skin SCC cells by downregulating the expression of several target genes with potential cancer promoting properties, including MMP-13, and by reducing SCC cell invasion. These results provide evidence that MMP-13 potently regulates cell viability, myofibroblast function and angiogenesis associated with wound healing and cancer. In addition, fibroblasts expressing MMP-13 show high collagen reorganization capacity. Moreover, the results suggest that KGF mediates the anti-cancer effects on skin SCC
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The RECK gene was initially isolated as a transformation suppressor gene encoding a novel membrane-anchored glycoprotein and later found to suppress tumor invasion and metastasis by regulating matrix metalloproteinase-9. Its expression is ubiquitous in normal tissues, but undetectable in many tumor cell lines and in fibroblastic lines transformed by various oncogenes. The RECK gene promoter has been cloned and characterized. One of the elements responsible for the oncogene-mediated downregulation of mouse RECK gene is the Sp1 site, where the Sp1 and Sp3 factors bind. Sp1 transcription factor family is involved in the basal level of promoter activity of many genes, as well as in dynamic regulation of gene expression; in a majority of cases as a positive regulator, or, as exemplified by the oncogene-mediated suppression of RECK gene expression, as a negative transcription regulator. The molecular mechanisms of the downregulation of mouse RECK gene and other tumor suppressor genes are just beginning to be uncovered. Understanding the regulation of these genes may help to develop strategies to restore their expression in tumor cells and, hence, suppress the cells' malignant behavior.
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Reports remain insufficient on whether and how prostate-specific membrane antigen (PSMA) can influence in vivo osseous metastasis of prostate cancer (PCa). In the present study, the authors induced stable expression of PSMA in mouse PCa cell line RM-1. In vivo osseous metastasis was induced in 37 6-week-old female C57BL/6 mice weighing 22.45 0.456 g. RM-1 cells were actively injected into the femoral bone cavity, leading to bilateral dissymmetry of bone density in the femoral bone. Tumor cells were also detected in bone tissue by pathological examination. The impact on bone density was demonstrated by the significant difference between animals injected with RM-PSMA cells (0.0738 0.0185 g/cm) and animals injected with RM-empty plasmid cells (0.0895 0.0241 g/cm). The lytic bone lesion of the RM-PSMA group (68.4%) was higher than that of the control group (27.8%). Immunohistochemistry showed that the expression of both vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9 (MMP-9) was distinctly higher in the RM-PSMA group than in the control group, while ELISA and Western blot assay indicated that VEGF and MMP-9 were higher in the RM-PSMA group compared to the control group (in vitro). Thus, the present study proposed and then confirmed for the first time that PSMA can promote in vivo osseous metastasis of PCa by increasing sclerotic destruction of PCa cells. Further analyses also suggested that PSMA functions positively on the invasive ability of RM-1 by increasing the expression of MMP-9 and VEGF by osseous metastases in vivo
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Chronic inflammation induced by amyloid-beta (Aβ) plays a key role in the development of age-related macular degeneration (AMD), and matrix metalloproteinase-9 (MMP-9), interleukin (IL)-6, and IL-8 may be associated with chronic inflammation in AMD. Sirtuin 1 (SIRT1) regulates inflammation via inhibition of nuclear factor-kappa B (NF-κB) signaling, and resveratrol has been reported to prevent Aβ-induced retinal degeneration; therefore, we investigated whether this action was mediated via activation of SIRT1 signaling. Human adult retinal pigment epithelial (RPE) cells were exposed to Aβ, and overactivation and knockdown of SIRT1 were performed to investigate whether SIRT1 is required for abrogating Aβ-induced inflammation. We found that Aβ-induced RPE barrier disruption and expression of IL-6, IL-8, and MMP-9 were abrogated by the SIRT1 activator SRT1720, whereas alterations induced by Aβ in SIRT1-silenced RPE cells were not attenuated by SRT1720. In addition, SRT1720 inhibited Aβ-mediated NF-κB activation and decrease of the NF-κB inhibitor, IκBα. Our findings suggest a protective role for SIRT1 signaling in Aβ-dependent retinal degeneration and inflammation in AMD.
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We aimed to investigate the effects of an anti-tumor necrosis factor-α antibody (ATNF) on cartilage and subchondral bone in a rat model of osteoarthritis. Twenty-four rats were randomly divided into three groups: sham-operated group (n=8); anterior cruciate ligament transection (ACLT)+normal saline (NS) group (n=8); and ACLT+ATNF group (n=8). The rats in the ACLT+ATNF group received subcutaneous injections of ATNF (20 μg/kg) for 12 weeks, while those in the ACLT+NS group received NS at the same dose for 12 weeks. All rats were euthanized at 12 weeks after surgery and specimens from the affected knees were harvested. Hematoxylin and eosin staining, Masson's trichrome staining, and Mankin score assessment were carried out to evaluate the cartilage status and cartilage matrix degradation. Matrix metalloproteinase (MMP)-13 immunohistochemistry was performed to assess the cartilage molecular metabolism. Bone histomorphometry was used to observe the subchondral trabecular microstructure. Compared with the rats in the ACLT+NS group, histological and Mankin score analyses showed that ATNF treatment reduced the severity of the cartilage lesions and led to a lower Mankin score. Immunohistochemical and histomorphometric analyses revealed that ATNF treatment reduced the ACLT-induced destruction of the subchondral trabecular microstructure, and decreased MMP-13 expression. ATNF treatment may delay degradation of the extracellular matrix via a decrease in MMP-13 expression. ATNF treatment probably protects articular cartilage by improving the structure of the subchondral bone and reducing the degradation of the cartilage matrix.
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Le syndrome de Wernicke-Korsakoff (SWK) est un dsordre neuropsychiatrique caus par la dficience en thiamine (DT). Dans la DT exprimentale comme dans le SWK, on observe une mort neuronale et des hmorragies dans certaines rgions prcises du diencphale et du tronc crbral. Les lsions diencphaliques du SWK sont particulirement svres et entranent souvent des squelles amnsiques permanentes. Le lien entre la dysfonction mtabolique induite par la DT et la mort neuronale nest pas connu. Des rapports prcdents ont dmontr que la permabilit de la barrire hmato-encphalique (BHE) tait altre et ce, prcdant lapparition du dommage neuronal, suggrant un rle critique de la dysfonction vasculaire. Les jonctions serres (JS) interendothliales, la base anatomique de la BHE, constituent un rseau molculaire incluant loccludin et les zonula occludens (ZOs). Cette thse dmontre une perte dexpression et une altration de la morphologie de ces protines en relation avec la dysfonction de la BHE dans le thalamus de souris dficientes en thiamine, fournissant une explication pour la prsence dhmorragies. Le stress oxydatif peut entraner des dommages directs aux protines des JS et interfrer avec leurs mcanismes de rgulation. De plus, loxyde nitrique (NO) peut induire la mtalloprotinase matricielle-9 (MMP-9) implique dans la dgradation de ces protines. Lendothlium vasculaire crbral (EVC) semble tre une source importante de NO dans la DT, lexpression de loxyde nitrique synthase endothliale (eNOS) tant slectivement induite dans les rgions vulnrables. Le NO peut ragir avec les espces ractives oxygnes et former du peroxynitrite, entranant un stress oxydatif/nitrosatif endothlial. Les rsultats prsents dmontrent que la dltion du gne de eNOS prvient le stress oxydatif/nitrosatif crbrovasculaire, lextravasation des immunoglobulins G (IgGs) et laltration de loccludin et des ZOs dans le thalamus de souris dficientes en thiamine. De plus, cette dltion prvient linduction de lexpression de MMP-9 dans lEVC. Des rsultats similaires ont t obtenus avec lantioxydant N-actylcystine (NAC). Les mcanismes prcis par lesquels les espces ractives altrent les protines des JS sont inconnus. Caveolin-1, une composante majeure du caveol de lEVC, est implique dans la rgulation de lexpression des protines des JS, et celle-ci est module par le stress oxydatif/nitrosatif; laltration de lexpression de caveolin-1 a t rcemment associe la rupture de la BHE. Les rsultats prsents dmontrent que lexpression de caveolin-1 est slectivement altre dans lEVC du thalamus de souris dficientes en thiamine, cocidant avec la rupture de la BHE, et dmontrent que la normalisation de lexpression de caveolin-1 par le NAC est associe avec lattnuation du dommage la BHE. Pris ensemble, ces rsultats dmontrent un rle central du stress oxydatif/nitrosatif crbrovasculaire, particulirement celui provenant de eNOS, dans laltration des JS de la BHE via des dommages directs et via linduction de MMP-9 et de caveolin-1. Cette rupture de la BHE contribue par consquent la mort neuronale dans le thalamus, puisque la prvention des altrations crbrovasculaires par la dltion du gne de eNOS et le NAC attnue significativement la mort neuronale. Ladministration prcoce dantioxydants en combinaison avec la thiamine devrait donc tre une considration importante pour le traitement du SWK.
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Le cartilage est un tissu conjonctif compos dune seule sorte de cellule nomme chondrocytes. Ce tissu offre une fondation pour la formation des os. Les os longs se dveloppent par l'ossification endochondral. Ce processus implique la coordination entre la prolifration, la diffrenciation et l'apoptose des chondrocytes, et rsulte au remplacement du cartilage par l'os. Des anomalies au niveau du squelette et des dfauts lis lge tels que larthrose (OA) apparaissent lorsquil y a une perturbation dans lquilibre du processus de dveloppement. ce jour, les mcanismes exacts contrlant la fonction et le comportement des chondrocytes pendant la croissance et le dveloppement du cartilage sont inconnus. Le rcepteur activateur de la prolifration des peroxysomes (PPAR) gamma est un facteur de transcription impliqu dans l'homostasie des lipides. Plus rcemment, son implication a aussi t suggre dans l'homostasie osseuse. Cependant, le rle de PPAR in vivo dans la croissance et le dveloppement du cartilage est inconnu. Donc, pour la premire fois, cette tude examine le rle spcifique de PPAR in vivo dans la croissance et le dveloppement du cartilage. Les souris utilises pour ltude avaient une dltion conditionnelle au cartilage du gne PPAR. Ces dernires ont t gnres en employant le systme LoxP/Cre. Les analyses des souris ayant une dltion au PPAR aux stades embryonnaire et adulte dmontrent une rduction de la croissance des os longs, une diminution des dpts de calcium dans los, de la densit osseuse et de la vascularisation, un dlai dans lossification primaire et secondaire, une diminution cellulaire, une perte dorganisation colonnaire et une diminution des zones hypertrophiques, une dsorganisation des plaques de croissance et des chondrocytes dforms. De plus, la prolifration et la diffrenciation des chondrocytes sont anormales. Les chondrocytes et les explants isols du cartilage mutant dmontrent une expression rduite du facteur de croissance endothlial vasculaire (VEGF)-A et des lments de production de la matrice extracellulaire. Une augmentation de lexpression de la mtalloprotinase matricielle (MMP)-13 est aussi observe. Dans les souris ges ayant une dltion au PPAR, y est aussi not des phnotypes qui ressemblent ceux de lOA tel que la dgradation du cartilage et l'inflammation de la membrane synoviale, ainsi quune augmentation de lexpression de MMP-13 et des nopitopes gnrs par les MMPs. Nos rsultats dmontrent que le PPAR est ncessaire pour le dveloppement et lhomostasie du squelette. PPAR est un rgulateur essentiel pour la physiologie du cartilage durant les stades de croissance, de dveloppement et de vieillissement.
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Introduction: Lactivation des cellules stellaires hpatiques (CSHs) est un point cl du processus de fibrose hpatique. Les lymphocytes T CD4+ intra-hpatiques sont une source majeure de cytokines anti-inflammatoires comme lIL-10 et pro-inflammatoire (IL-17A), hpatoprotectrice (IL-22) produites par les Th17. Les Th17 sont impliqus dans de nombreuses pathologies inflammatoires mais leffet de ces cellules sur les CSHs nest pas encore lucid. Objectif: Comprendre le rle des cytokines de type Th17 dans le processus dactivation des CSHs. Mthodes: La ligne de CSHs humaine LX2 a t stimule par lIL-17A ou lIL-22 puis compare des cellules traites par le TGF-b et le tampon phosphate salin (PBS). Lactivation des CSHs a t value en examinant les molcules profibrotique alpha-smooth muscle actin (a-SMA), collagne de type I (COL1A1) et inhibiteur produits par les tissus des mtalloprotases matricielles I (TIMP-I) par q-PCR. Lexpression protique a t valide par immunobuvardage ou coloration au rouge de picro Sirius. Lexpression membranaire de lIL-10Rb, du TGF-b-RII et de lIL-17RA a t mesure par cytomtrie en flux. Rsultats: LIL-17A et lIL-22 nactivent pas les cellules LX2, car aucune induction da-SMA, de COL1A1 et de TIMP-I na t observe. Cependant, lIL-17A et lIL-22 sensibilisent les CSHs laction du TGF-b, tel que dmontr par une forte expression et production da-SMA, collagne type I et TIMP-I. LIL-17A, mais pas lIL-22, induit la surexpression la surface cellulaire du TGF-b-RII et inhibe partiellement la baisse dexpression du TGF--RII aprs stimulation au TGF-b. Conclusion: Nos rsultats dmontrent une fonction pro-fibrotique de lIL-17A et de lIL-22, car les deux cytokines sensibilisent les CSHs laction du TGF-b. LIL-17A agit via la surexpression et la stabilisation du TGF-b-RII tandis que lIL-22 agit probablement par des mcanismes intracellulaires.
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La dgradation protolytique du collagne de type II est considre comme tant un facteur majeur dans le processus irrversible de dgradation de la matrice cartilagineuse lors dostoarthrose. Outre les collagnases de la famille des mtaloprotinases de la matrice (MMP-1, -8, -13), la cathepsine K est parmi les seules enzymes susceptibles de dgrader la triple hlice intacte du collagne de type II, devenant ainsi un lment pertinent pour les recherches sur lostoarthrose. Lobjectif court terme de notre tude consiste en lidentification et la caractrisation de sites de clivage spcifiques de la cathepsine K sur le collagne de type II quin. La technique dlectrophorse SDS-PAGE 1D permet la visualisation des produits de digestion et la validation des rsultats de la caractrisation molculaire des fragments protolytiques. La caractrisation est ralise en combinant la digestion trypsique prcdant lanalyse HPLC-ESI/MS. Les rsultats ont permis dtablir les sites, prsents sur la carte peptidique de la molcule de collagne de type II quin, des 48 rsidus prolines (P) et 5 rsidus lysines (K) supportant une modification post-traductionnelle. De plus, 6 fragments majeurs, diffrents de ceux produits par les MMPs, sont observs par SDS-PAGE 1D puis confirms par HPLC-ESI/MS, correspondant aux sites suivants : F1 [G189-K190], F2 [G252-P253], F3 [P326-G327], F4 [P428-G429], F5 [P563-G564] et F6 [P824-G825]. Le fragment F1 nouvellement identifi suggre un site de clivage diffrent de ltude antrieure sur le collagne de type II bovin et humain. Lobjectif long terme serait le dveloppement danticorps spcifiques au site identifi, permettant de suivre lactivit protolytique de la cathepsine K par immunohistochimie et LISA, dans le cadre du diagnostic de lostoarthrose.
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Epidemiological studies have suggested an inverse correlation between red wine consumption and the incidence of CVD. However, Champagne wine has not been fully investigated for its cardioprotective potential. In order to assess whether acute and moderate Champagne wine consumption is capable of modulating vascular function, we performed a randomised, placebo-controlled, cross-over intervention trial. We show that consumption of Champagne wine, but not a control matched for alcohol, carbohydrate and fruit-derived acid content, induced an acute change in endothelium-independent vasodilatation at 4 and 8 h post-consumption. Although both Champagne wine and the control also induced an increase in endothelium-dependent vascular reactivity at 4 h, there was no significant difference between the vascular effects induced by Champagne or the control at any time point. These effects were accompanied by an acute decrease in the concentration of matrix metalloproteinase (MMP-9), a significant decrease in plasma levels of oxidising species and an increase in urinary excretion of a number of phenolic metabolites. In particular, the mean total excretion of hippuric acid, protocatechuic acid and isoferulic acid were all significantly greater following the Champagne wine intervention compared with the control intervention. Our data suggest that a daily moderate consumption of Champagne wine may improve vascular performance via the delivery of phenolic constituents capable of improving NO bioavailability and reducing matrix metalloproteinase activity.
