Дисертації з теми "Permeabilità intestinale"
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Ponce, de Leon Rodriguez Maria del Carmen. "Développement d’un modèle in vitro d’inflammation intestinale par l’utilisation de lignées cellulaires humaines en co-culture pour l’étude des interactionsavec les micro-constituants alimentaires." Thesis, Montpellier, 2019. http://www.theses.fr/2019MONTG009/document.
Повний текст джерелаThe intestinal epithelium, main place of the absorption of (micro)-nutrients is also the first body's defense system. An imbalance in homeostasis can lead to an inflammatory reaction associated with defects in the intestinal barrier and immune function as well as malabsorption of nutrients, as seen in IBD (Inflammatory Bowel Diseases), in micronutrient fortification strategies and noncommunicable diseases (obesity). It is therefore important to find ways of action, for example through diet, to prevent or at least reduce the nutritional and pathological consequences of intestinal inflammation, and to understand the mechanisms involved. Among intestinal models, in vitro cell culture models are increasingly used and allow to evaluate the molecular mechanisms in a simple and reproducible way and to reduce animal experimentation.In this context and in order to study the interaction of dietary bioactive compounds with the intestine in state of inflammation, the first objective of this work was the development of an in vitro model of inflamed intestine combining in co-culture two human intestinal cell lines: Caco-2 TC7 (enterocytes) and HT29-MTX (goblet cells) and an immune cell line of macrophages (THP1). Several inflammation markers were evaluated and we were able to show that the tri-culture model responded to an inflammatory stimulus (LPS / IFNγ), by increasing the production of pro-inflammatory cytokines (TNF-α, IL6 and IL8) and enzymes (INOS and COX2) as well as the expression of their genes. In addition, an increase of epithelial permeability via tight junctions (TJs) alteration has also been demonstrated, as well as overproduction of mucus, which are recognized inflammation characteristics.The second objective was to study the interaction of β-cryptoxanthin (BCX), a lipophilic and antioxidant carotenoid of citrus, with the inflamed model. To solubilize BCX, we used two types of micelles (artificial and physiological) and studied markers of inflammation. Although it appears from the preliminary results that BCX micelles show a tendency to decrease the production of some cytokines (IL6 and IL8), the role of micelle constituents (Tween 40 or bile salts / phospholipids) in the phenomenon observed and in the epithelial permeability remains to be therefore clarified
Weaver, Laurence Trevelyan. "The intestinal permeability of infants." Thesis, University of Cambridge, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289788.
Повний текст джерелаSmethurst, Paul R. "Small intestinal permeability in man." Thesis, Open University, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.315531.
Повний текст джерелаLundin, Pål. "Intestinal permeability a parameter of mucosal dysfunction /." Lund : Dept. of Animal Physiology, Lund University, 1997. http://books.google.com/books?id=wuNqAAAAMAAJ.
Повний текст джерелаLang, Mia E. "Intestinal permeability in the irradiated ferret." Thesis, University of Ottawa (Canada), 1991. http://hdl.handle.net/10393/7772.
Повний текст джерелаAnderson, Alexander Douglas Gray. "Measurement of intestinal permeability in surgical patients." Thesis, University of Edinburgh, 2004. http://hdl.handle.net/1842/24575.
Повний текст джерелаSalameh, Emmeline. "Développement d'un modèle murin de dénutrition avec entéropathie et évaluation de molécules d'intérêt permettant de contribuer au rétablissement de la fonction de barrière intestinale." Thesis, Normandie, 2019. http://www.theses.fr/2019NORMR064.
Повний текст джерелаBackground : Severe acute malnutrition (SAM) is a global health issue affecting 17 million children under the age of 5. SAM induces rapid weight loss and is often associated with environmental enteric dysfunction (EED). EED is characterized by intestinal hyperpermeability and inflammation, villus blunting and nutrient malabsorption. EED might, therefore, limit stabilization and re-nutrition protocol efficacy. Objectives : This thesis aimed to develop an undernutrition model with enteropathy to evaluate the effect of a therapeutic milk enriched with nutrients on gut barrier function. Results : During preclinical model development, several approaches were tested: calorie restriction, low-protein diet, use of lipopolysaccharides and indomethacin. Only daily indomethacin gavage during one week in protein-energy undernourished mice induced growth faltering associated with enteropathy. After preclinical model validation, we evaluated the effect of therapeutic milk supplemented with glutamine, leucine, gum arabic and/or selenium-enriched yeast on gut barrier function. Glutamine and leucine induce beneficial effects on gut barrier function. In ourexperimental conditions, therapeutic milk enriched with a combination of glutamine and leucine had a limited impact on this parameter. Gum arabic and selenium-enriched yeasts have prebiotic and probiotic properties on gut barrier function. Therapeutic milk supplemented with gum arabic and selenium-enriched yeast inhibited intestinal inflammation and enhanced specific bacteria abundance such as Faecalibacterium prausnitzii.Conclusion : The studies conducted during this thesis permitted to develop a new model of undernutrition with enteropathy. Therapeutic milk enriched with arabic gum and selenium-enriched yeast triggered beneficial effects on gut barrier function in our preclinical model
Yao, Shengtao. "The effect of denervation on intestinal permeability and function following small intestinal transplantation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/mq22692.pdf.
Повний текст джерелаWang, Chuan. "Pathologically and experimentally induced intestinal barrier changes evaluated by permeability measurements." Lund : Dept. of Animal Physiology, Lund University, 1995. http://books.google.com/books?id=ddlqAAAAMAAJ.
Повний текст джерелаBahlouli, Wafa. "Régulation de la perméabilité intestinale au cours du syndrome de l'intestin irritable : role du système ubiquitine-protéasome et impact de l'obésité." Thesis, Normandie, 2019. http://www.theses.fr/2019NORMR047.
Повний текст джерелаIrritable bowel syndrome (IBS) is a multifactorial functional disorder, involving environmental factors (stress and diet for instance), gut-brain-axis dysfunction, micro-inflammation, dysbiosis and an alteration of intestinal permeability. The role of the proteasome in the regulation of the intestinal barrier during IBS has been studied. In addition, these intestinal functional disorders have also been described in patients with obesity. Nevertheless, the mechanisms underlying an association of intestinal functional disorders in the obesity context, remain poorly understood and have therefore been investigated in this thesis. In this study, "IBS-like" mouse models such as water avoidance stress (WAS) and the post-inflammatory (post-TNBS) models, were used to study the impact of proteasome inhibition on the regulation of intestinal permeability. We found that the pharmacological inhibition of the proteasome (with PR-957) or the use of knock-out mice for a subunit of the proteasome (β2i -/-) limit intestinal hyperpermeability occured in IBS-Like models. Moreover, we found that oral supplementation with glutamine also reduces intestinal hyperpermeability, wich, thus, can be considered as a putative nutritional treatment for IBS. A colonic proteomic study of WAS mice and a study of colonic ubiquitoma in IBS patients with diarrheal profiles confirmed the involvement of proteasome in the pathophysiology of IBS. Therefore, the link between obesity and IBS was examined by combining models of obesity (ob/ob genetic and high-fat diet [HFD] models) with WAS model. Only HFD mice displayed enhanced intestinal hyperpermeability and higher plasma corticosterone levels in response to WAS. Further studies suggest that these results, themselve, are independent of leptin, glycaemia and gut microbiota. This study paves new ways of treating patients suffering from IBS, by nutritional intervention via glutamine or by using the proteasome as a therapeutic target. We also suggest a role of diet (high fat) in the development of intestinal functional disorders during obesity
Benoit, Bérengère. "Effet des acides gras alimentaires à chaîne longue sur la barrière épithéliale colique." Thesis, Lyon 1, 2013. http://www.theses.fr/2013LYO10239.
Повний текст джерелаIntestinal goblet cells secrete mucins, mainly MUC2, which form a protective mucus gel. Despite the important place of long chain fatty acids (LCFA) in the diet and their links with pathologies where goblet cells are altered, there is no study dealing with their impact on goblet cells. The aim of my work was to highlight these interactions and to study their consequences. In vitro, we show that saturated LCFA increase MUC2 expression and release whereas unsaturated LCFA inhibit these process and that palmitic acid promotes cellular differentiation. In vivo, rat pups receiving oral administration of palm oil show a decrease of colonic paracellular permeability and an increase of MUC2 production. On the opposite, rapeseed and sunflower oils do not change MUC2 production and, intestinal permeability is the same as controls despite the increase of occludin expression. In an animal model of irritable bowel syndrome, palm oil effects are found again. When subjected rat pups to a maternal deprivation stress a few days after birth, they develop an intestinal hyperpermeability and a goblet cell depletion. We show that oral administration of palm oil concomitantly to the stress is able to, despite a decrease of occludin expression, restore the permeability at the level of non-stressed animals and to increase goblet cell number. Rapeseed oil and sunflower oil are not able to correct the increase of intestinal permeability. In parallel, studies in mice show that some types of diets can be associated with an increase of the number of proximal and distal goblet cells. To conclude, this work (i) helped to identify LCFA as nutrients able to modulate intestinal goblet cell number and physiology, (ii) put forward a new therapeutic track, via palmitic acid use, to restore goblet cell populations and intestinal permeability in pathologies associated with these kind of alterations and finally (iii) offered new tracks of reasoning about physiological and pathophysiological impacts of the increase of intestinal goblet cell number in a healthy subject
Stenberg, Patric. "Computational models for the prediction of intestinal membrane permeability." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2001. http://publications.uu.se/theses/91-554-4934-4/.
Повний текст джерелаAlhamoruni, Abdissalam Ag Ali. "In vitro studies of huam intestinal permeability and modulation." Thesis, University of Nottingham, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.537654.
Повний текст джерелаGenser, Laurent. "Etude de la perméabilité intestinale au cours de l'obésité humaine." Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066645.
Повний текст джерелаIntestinal barrier damage is associated with low-grade inflammation and metabolic impairment in rodent models of obesity. Whether intestinal permeability is altered in human metabolic disorders remains poorly investigated. Using a large cohort of well-characterized obese subjects and a human enterocyte model, we examined intestinal permeability in the basal state and after a challenge by a lipid load. We showed a reduction of occludin and tricellulin at jejunal tight junctions and increased serum levels of zonulin and LPS-Binding Protein in obese subjects. Jejunal permeability, directly measured in Ussing chambers in the fasting condition, was not significantly increased compared to non-obese subjects. Nevertheless, within the obese cohort, high permeability was associated with systemic inflammation (CRP and haptoglobin). A single lipid load increased permeability both in Caco-2/TC7 cells and ex vivo in human jejunum, demonstrating dietary lipids’ direct effects on the epithelial barrier. Permeability after the lipid load was significantly higher in the jejunum of obese subjects and associated with systemic and intestinal inflammation (CRP and fecal calprotectin) and type 2 diabetes. Thus, our results highlight an intestinal barrier defect in obesity, with a jejunal permeability increased by a lipid challenge and linked to inflammatory and metabolic impairments
ANCEL, DAVID BIGARD MARC-ANDRE. "COMPARAISON DE LA PERMEABILITE INTESTINALE ENTRE CIRRHOSE ETHYLIQUE ET CIRRHOSE VIRALE." [S.l.] : [s.n.], 2001. http://www.scd.uhp-nancy.fr/docnum/SCDMED_T_2001_ANCEL_DAVID.pdf.
Повний текст джерелаYadav, Vipul. "Intestinal stability and permeability of anti-TNF α monoclonal antibodies". Thesis, University College London (University of London), 2017. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.724210.
Повний текст джерелаWillemsen, Linette Eustachia Maria. "Intestinal barrier function: regulation of epithelial permeability and mucin expression." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2004. http://dare.uva.nl/document/74526.
Повний текст джерелаHoorelbeke, Anne. "Evaluation de la scintigraphie de permeabilite alveolaire et intestinale dans la sclerodermie." Lille 2, 1991. http://www.theses.fr/1991LIL2M303.
Повний текст джерелаDIAMANTE, BARBARA. "PROPRIETA' FUNZIONALI DELLA BARRIERA INTESTINALE DI INSETTO E MODULAZIONE DELLA PERMEABILITA' PARACELLULARE." Doctoral thesis, Università degli Studi di Milano, 2012. http://hdl.handle.net/2434/168386.
Повний текст джерелаZamora, Samuel A. "Crohn's disease, investigation of intestinal permeability across families of affected children." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/mq24714.pdf.
Повний текст джерелаTannergren, Christer. "Intestinal Permeability and Presystemic Extraction of Fexofenadine and R/S-verapamil." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3971.
Повний текст джерелаRuttenberg, David. "Intestinal permeability to polyethylene glycol 400 in patients with Crohn's disease." Master's thesis, University of Cape Town, 1993. http://hdl.handle.net/11427/25587.
Повний текст джерелаRubelt, Miriam. "Enhancement of the intestinal epithelial permeability of peripherally acting opioid analgesics by chitosan." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2013. http://dx.doi.org/10.18452/16864.
Повний текст джерелаAnalgesic effects of opioids are mediated by opioid receptors that are widely distributed in the central and peripheral nervous systems (CNS and PNS, respectively). Although opioids are the most powerful analgesics, severe side effects restrict their use and affect patient convalescence. This suggests an advantage of new analgesic opioids which selectively bind to opioid receptors in the PNS. After oral administration however, peripherally restricted opioids first have to cross the intestinal epithelial barrier before absorption into the circulation and distribution to opioid receptors in peripheral tissues. Here, the transport across intestinal epithelia of two opioid ligands (AS006 and loperamide) that selectively activate peripheral opioid receptors without entering the CNS were investigated. To increase the intestinal passage of these drugs, the absorption enhancer chitosan was used. Chitosan significantly decreased the transepithelial resistance of HT29/B6 and Caco-2 cell monolayers after 30 min in vitro. The permeability values for AS006 increased from < 0.3 × 10-6 cm/s up to 10 × 10-6 cm/s in the presence of chitosan. In contrast, HT29/B6 monolayers showed moderate loperamide permeability in the presence of chitosan, and chitosan had no effect on the permeability of loperamide using Caco-2 monolayers. Oral administration of loperamide induced a dose-depended elevation of paw pressure thresholds in inflamed paws that lasted for 60 min. Oral administration of loperamide combined with chitosan slightly but nonsignificantly enhanced the antinociceptive effect of loperamide. In conclusion, chitosan is a suitable absorption enhancer for in vitro intestinal permeability studies. Future in vivo experiments might investigate different formulations and application schedules, and further address the effects of chitosan on the antinociceptive efficacy of hydrophilic opioids.
COLLET, REGIS. "Anomalies de la permeabilite pulmonaire dans la maladie de crohn : relations avec la permeabilite intestinale et le lavage broncho-alveolaire." Lille 2, 1989. http://www.theses.fr/1989LIL2M307.
Повний текст джерелаHøst, Jan. "In silico predicition of intestinal transport /." Cph. : The Danish University of Pharmaceutical Sciences, 2006. http://www.dfuni.dk/index.php/Jan_Hoest/3066/0/.
Повний текст джерелаBours, Martijn Jan Leo. "Role of extracellular ATP in immunity and intestinal defence effects on intestinal permeability and enterocyte-driven inflammatory response /." Maastricht : Maastricht : Universitaire Pers Maastricht ; University Library, Universiteit Maastricht [host], 2007. http://arno.unimaas.nl/show.cgi?fid=9328.
Повний текст джерелаBajka, Balazs Hendrik. "The characterization of an in vitro model of small intestinal permeability dysfunction /." Title page and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09SB/09sbb165.pdf.
Повний текст джерелаCASULA, EMANUELA. "Probiotic Lactobacillus strains attenuate oxysterols-induced alteration of human intestinal membrane permeability." Doctoral thesis, Università degli Studi di Cagliari, 2021. http://hdl.handle.net/11584/312980.
Повний текст джерелаAdenis, Antoine. "Etude de la permeabilite intestinale et pulmonaire au cours de la maladie de crohn." Lille 2, 1989. http://www.theses.fr/1989LIL2M097.
Повний текст джерелаFoster, Russell. "Modulation of intestinal permeability with special reference to the absorption of bioactive peptides." Thesis, King's College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.281711.
Повний текст джерелаGertz, Michael. "Prediction of intestinal availability in human from in vitro clearence and permeability data." Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.503642.
Повний текст джерелаTRISAL, PREETI. "IMPACT OF NONIONIZABLE GLYCOL SOLUBILIZERS EXHIBITING DIFFERENT SURFACE ACTIVITIES ON INTESTINAL MEMBRANE PERMEABILITY." University of Cincinnati / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1116005486.
Повний текст джерелаBidu, Célia. "Résistance des souris transgéniques fat-1 à l'obésité : prévention de l'endotoxémie métabolique et modulation du microbiote intestinal par les acides gras polyinsaturés en n-3." Thesis, Dijon, 2015. http://www.theses.fr/2015DIJOS058/document.
Повний текст джерелаObesity is associated with chronic low-grade inflammatory state and secondary metabolicdisorders, such as insulin-resistance, glucose intolerance and hepatic steatosis. Gut microbiotaseems to play an important role in these obesity features. Moreover, microbiota dysbiosis has beenshown to be associated with increased systemic lipopolysaccharides levels, called metabolicendotoxemia. N-3 PUFAs are anti-obesity and anti-inflammatory molecules able to modulate gutmicrobiota and prevent metabolic endotoxemia. We showed that fat-1 transgenic mice,endogenously synthetizing n-3 PUFAs, resist to obesity development and comorbidities whensubmitted to diet-induced obesity for 18 weeks. These mice exhibit a maintained intestinal barrierfunction and a prevention of metabolic endotoxemia. Moreover, cecal microbiota analysis revealedan increase of Akkermansia phylum. Microbiota transplantation of fat-1 mice to wild type micewas shown to exert protective effects against diet-induced obesity and associated disorders. Thus,increasing gut microbiota Akkermansia population by appropriate n-3 PUFAs may represent apromising strategy to prevent obesity, insulin-resistance, glucose intolerance and hepatic steatosis
Esser, Dirk Michael [Verfasser]. "Veränderungen der intestinalen Permeabilität bei operierten Morbus Crohn Patienten / Dirk Michael Esser." Köln : Deutsche Zentralbibliothek für Medizin, 2010. http://d-nb.info/1001963970/34.
Повний текст джерелаChamignon, Célia. "Identification de souches bactériennes à potentiel probiotique dans la diminution des hyperperméabilités intestinales et détermination de leur(s) mécanisme(s) d’action." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASA011.
Повний текст джерелаThe gastro-intestinal tract represents the largest interface between the human body and its environment. It is a multilayer system composed of mucus and epithelial cells that establish and regulate barriers, while directly connecting to the immune system. This interface allows fluxes of water and nutriments and prevents from the entry of antigens and pathogens. Thus, it is the first line of defense. The regulation of the permeability occurs through the paracellular pathway, which is supported by the epithelial complex of junctional proteins. The gut microbiota also plays a key role in the regulation of the immune and metabolic systems and also, in the protection against pathogens. The continuous cross-talks between the intestinal barrier and the microbiota are essential to maintain the intestinal integrity and therefore the global homeostasis in healthy conditions. Nowadays, most of the chronic syndromes and diseases, such as irritable bowel syndrome (IBS) but also metabolic or behavioral disorders, are associated with an increase of the gut permeability also called “leaky gut syndrome”. Indeed, the consequence of the hyperpermeability is a flow increase of water and nutriments across the intestinal barrier but also of pathogens or toxins, among others, promoting an immune response and inflammation. Many studies also associated changes in the gut microbiota composition, dysbiosis, with chronic diseases. The beneficial effects of probiotic strains are increasingly demonstrated from in vitro experimentations to clinical trials and these studies demonstrated that they can be used in both the prevention and treatment of these disorders. We aimed to better decipher the interactions between the intestinal epithelial components and the probiotic bacteria in the pathophysiological context of intestinal chronic disorders. To do that, we first designed an in vitro screening of over fifty strains, from different genus, based on trans-epithelial electrical resistance (TEER) of two types of human intestinal epithelial cell lines, Caco-2 and T84. With these models, six Lactobacillus strains were selected and we better characterized their probiotic properties (adhesion ability, biofilm stability, neurotransmitter production and enzyme activity). We further evaluated the effect of four of them in in vivo models of chronic low-grade inflammation and neonatal maternal separation using C57BL/6J mice. Finally, we determined the implication of the bacterial strains in the modulation of the gut permeability, through the study of the complex of cellular junctional proteins
Schuster, Stephanie Ann Foley Joe Preston. "Electrokinetic chromatography using novel unilamellar vesicles for unique separations and prediction of intestinal permeability /." Philadelphia, Pa. : Drexel University, 2007. http://hdl.handle.net/1860/2579.
Повний текст джерелаDemirbas, Ucpinar Sibel. "Oligonucleotides and protease inhibitors transport across CaCo-2 cell monolayers-permeability effects of dimethylsulfoxide and citicholine /." Full text (PDF) from UMI/Dissertation Abstracts International, 2000. http://wwwlib.umi.com/cr/utexas/fullcit?p3004252.
Повний текст джерелаZhou, Yi. "Mechanisms of S-nitrosothiols intestinal permeability and NO store formation within vascular wall to improve NO oral delivery systems." Thesis, Université de Lorraine, 2019. http://www.theses.fr/2019LORR0101/document.
Повний текст джерелаS-nitrosothiols (RSNOs) such as S-nitrosoglutathione (GSNO) are promising nitric oxide (NO) donors for cardiovascular diseases treatment. However, they are poorly stable drug candidates. In previous studies, GSNO-loaded nanoparticles (GSNO-NP) were embedded into an alginate/chitosan matrix. Resulting nanocomposite particles showed high encapsulation and sustained release of GSNO, and led to the formation of a NO store in the wall of aorta after a single oral administration to rats. However, these nanocomposite particles have several limitations such as time-consuming preparation, lack of both stability and reproducibility. This thesis work aimed at: 1) Elucidate the mechanism of free RSNOs intestinal absorption; 2) Evaluate ability of free RSNOs to form a vascular NO store; 3) Optimize the GSNO formulation. In this study, we showed that the intestinal permeability (in vitro model of intestinal barrier) of GSNO, S-nitroso-N-acetylcysteine (NACNO) and S-nitroso-N-acetylpenicillamine (SNAP) was a passive diffusion, following the transcellular pathway (and also the paracellular way for SNAP) and belonging to the medium permeability class. After crossing the intestinal barrier, RSNOs will reach the vasculature. In order to compare the ability of free RSNOs to form a vascular store of NO either in endothelium-intact or endothelium-removed aortae, we quantified the store, verified its bioavailability for vasorelaxation and evaluated its impact on phenylephrine (PHE)-induced vasoconstriction. Incubation with RSNOs increased the basal NO store three to five times. This store is still bioavailable to induce vasorelaxation and efficient to induce vascular hyporeactivity to PHE (NACNO> GSNO = SNAP) only in endothelium-removed aortae. As intestinal permeability of RSNOs was in the medium class, the integration of GSNO into an appropriate delivery system is essential. Limitations of previously developed nanocomposites particles were impossible to bypass so the production process of GSNO-NP was modified (liquid or solid GSNO in the internal phase of the emulsion) to produce microparticles. Both kinds of microparticles exhibited a slower release of GSNO than GSNO-NP. Nano-and micro-particles were stable after lyophilization and presented an enhancement of GSNO intestinal permeability (up to high permeability class for microparticles). Thus, oral administration of GSNO/RSNO loaded nano/micro particles seems to be a promising avenue for the treatment of cardiovascular diseases
Chucta, Emily E. "LC-PUFA and sialyllactose modulation of intestinal permeability and the inflammatory response when challenged in the porcine intestinal cell line IPEC-J2." The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu156614954555964.
Повний текст джерелаDossou-Yovo, Flore. "Modification de la biodisponibilité orale des médicaments : interactions « Herb-Drugs » « Drugs- Drugs»." Thesis, Paris, CNAM, 2014. http://www.theses.fr/2014CNAM0936/document.
Повний текст джерелаOral dosing is still seen as the silver bullet of drug administration, as it is cheaper andbetter adapted to patient comfort. However, oral route is still inaccessible to many drugssuch as biologics and biosimilars respectively certain anticancer drugs and antiretrovirals(ARV).The aim of this present study was to find new drugs enhancers that improve the oralbioavailability of drugs and xenobiotics. All the studies were realized in vitro using Ussingchambers technic. To achieve the set objective we used the strategy to develop drugenhancer which can modulate at the same time transcellular and paracellular pathways.In the first part of this study (patent) we have shown that the use of a pharmaceutical and /or a dietetic formulation containing a plant extract (Hibiscus sabdariffa) could increase thebioavailability in vitro in rats not only of cisplatin (21 fold), oxaliplatin (11 fold) andFluorescein Isothiocyanate-Dextran 4000 (FD4, 3 fold). All that drugs were transportedthrough intestinal barrier using paracellular pathway. In addition the study showed thatthis formulated enhancer can increased the bioavailability of Efavirenz (7 fold) andAtazanavir (4 fold) which are active transported.In order to assess the effect of new drugs enhancer on mucus thickness that limits thetransport of xenobiotic through intestinal barrier, we decide to evaluate his effect on passiveand active transport of drugs.In the second part of this study we have shown that after a week of pre-treatment of ratswith Metronidazole (MTZ, publication 1) and Cotrimoxazole (CTX, publication 2), the twomost commonly used antibiotics in the prophylaxis against opportunistic infections in HIV /AIDS, both increase colonic mucus thickness that affect directly passive intestinalpermeability by reducing conductance an index of passive transport through intestinalepithelium. In addition those antibiotics also entail a change in the transepithelialconductance and ARV fluxes. After MTZ and CTX treatment the secretion of Atazanavir(ATZ) increases respectively in the proximal colon by 2 to 4 fold and in the distal colon by 3to 5 fold respectively. Ritonavir (RTV) is poorly absorbed in control, after a week of pretreatmentwith MTZ and CTX one rather notices a secretion of RTV 5 to 10 fold higher in theproximal and 2 to 5 fold higher in the distal colon. The next study will be conducted toevaluate the effect of new drugs enhancer on mucus thickness layer.In conclusion, oral bioavailability of drugs and xenobiotics can be enhanced bypharmaceutical composition that contains herbal extract which increase passive and activetransport of drugs through intestinal barrier
Denizot, Jérémy. "Perméabilité intestinale et régulation de l'expression du gène CEACAM6 : implication des bactéries Escherichia coli associées à la maladie de Crohn." Thesis, Clermont-Ferrand 1, 2013. http://www.theses.fr/2013CLF1MM04/document.
Повний текст джерелаNo abstract available
Jugan, Maria Christine. "Effects of Akkermansia muciniphila Supplementation on Markers of Intestinal Permeability in Dogs Following Antibiotic Treatment." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1488318772663017.
Повний текст джерелаGroschwitz, Katherine R. "Mast cell-mediated intestinal barrier function in homeostasis and disease." University of Cincinnati / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1291389792.
Повний текст джерелаFINCK, CAROLE. "Exploration de la permeabilite intestinale au cr 51-edta au cours des eczemas : notre experience a propos de 47 cas." Besançon, 1993. http://www.theses.fr/1993BESA3058.
Повний текст джерелаAllen, Hilary Kaye. "The Effects of Enteropathogenic and Commensal Escherichia coli on Tight Junction Permeability." Wright State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=wright1341611861.
Повний текст джерелаLe, Nga Thi Thanh. "Regulation of Intestinal Epithelial Barrier and Immune Function by Activated T Cells." Case Western Reserve University School of Graduate Studies / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=case1599833768774075.
Повний текст джерелаJuel, Ingebjørg S. "Intestinal injury and recovery after ishemia - An experimental study on restitution of the surface epithelium, intestinal permeability, and release of biomarkers from the mucosa." Doctoral thesis, Norwegian University of Science and Technology, Department of Cancer Research and Molecular Medicine, 2007. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-1817.
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Повний текст джерелаMcGilligan, Victoria. "The protective mechanisms of nicotine in relation to intestinal epithelial permeability and inflammation in ulcerative colitis." Thesis, University of Ulster, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.445045.
Повний текст джерелаFreitas, Antonio Klingem Leite de. "Efeito da SuplementaÃÃo com Alanil-Glutamina nas AlteraÃÃes da Permeabilidade Intestinal em Ratos Treinados Submetidos a um ExercÃcio Prolongado e Exaustivo de NataÃÃo." Universidade Federal do CearÃ, 2013. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=12375.
Повний текст джерелаO exercÃcio prolongado e exaustivo induz uma disfunÃÃo da barreira intestinal. VÃrios estudos mostram que a suplementaÃÃo com alanil-glutamina (A/G) melhora a proliferaÃÃo das cÃlulas intestinais e absorÃÃo de eletrÃlitos. O objetivo deste trabalho foi investigar o efeito da suplementaÃÃo com A/G na permeabilidade intestinal em ratos treinados apÃs um exercÃcio prolongado e exaustivo de nataÃÃo. Utilizamos ratos Wistar, divididos em sete grupos: 1) SedentÃrio (S); 2) SedentÃrio A/G (S-A/G); 3) Treinado (T); 4) Treinado A/G (T-A/G); 5) ExaustÃo (E); 6) ExaustÃo A/G (E-A/G) e 7) Recuperado (R). Os animais dos grupos suplementados receberam o dipeptÃdeo A/G. Os animais foram treinados durante 12 semanas de nataÃÃo. Na metodologia realizamos anÃlises bioquÃmicas de pH, pCO2, pO2, SO2, excesso de bases (BE), pelo mÃtodo de gasometria e lactato e glicose. Analisamos a transcriÃÃo das junÃÃes firmes: ZO-1, Ocludina, Claudina-2 e PEPT-1 atravÃs de RT-PCR. A anÃlise da permeabilidade intestinal foi realizada pelo mÃtodo da ingestÃo de Lactulose/Manitol (L/M). Fizemos tambÃm anÃlise histolÃgica do duodeno, jejuno e Ãleo. O presente estudo foi aprovado pela CEPA-UFC, em protocolo de N 13/13. Nossos resultados mostraram que pCO2 e SO2 foram aumentados nos grupos E e E-A/G, mas houve queda nos parÃmetros de pH e BE para estes mesmos grupos. Encontramos queda dos Ãndices de glicose e aumento das concentraÃÃes de lactato. Houve aumento significativo no percentual de excreÃÃo de lactulose nos grupos E e E-A/G em relaÃÃo ao grupo S. Houve, no entanto, queda da excreÃÃo de lactulose com diferenÃa estatÃstica entre os grupos E e E-A/G, mostrando proteÃÃo da A/G frente ao aumento da permeabilidade intestinal promovida pelo exercÃcio exaustivo. O percentual de excreÃÃo do manitol foi aumentado nos grupos E e E-A/G em relaÃÃo ao grupo S. Entretanto, na anÃlise da relaÃÃo da permeabilidade dos dois carboidratos L/M observamos um aumento significativo no grupo E em relaÃÃo ao grupo S. Contudo, houve diferenÃa significativa entre os grupos E e E-A/G mostrando que a A/G conseguiu reverter os efeitos da atividade exaustiva na permeabilidade intestinal. Observamos aumento da ZO-1 e ocludina nos grupos S-A/G e T em relaÃÃo a S. Houve tambÃm aumento de ZO-1 no grupo E em relaÃÃo ao S. PorÃm, a A/G reverteu à transcriÃÃo destas junÃÃes firmes nos grupos T-A/G e E-A/G. A transcriÃÃo de claudina-2 foi reduzida no grupo S-A/G, mas obtivemos um aumento no grupo E em relaÃÃo ao S e uma diminuiÃÃo de E-A/G em relaÃÃo ao E. Em relaÃÃo ao PEPT-1, observamos aumento da transcriÃÃo nos grupos T e E em relaÃÃo ao S. Contudo, a A/G reverteu à transcriÃÃo deste peptÃdeo no grupo E-A/G em relaÃÃo ao E. Numa anÃlise de 72 horas apÃs o teste de exaustÃo encontramos valores para a permeabilidade intestinal similares aos grupos sedentÃrios. ConcluÃmos que o exercÃcio prolongado e exaustivo alterou a permeabilidade intestinal e a suplementaÃÃo crÃnica com alanil-glutamina teve efeito protetor contra este aumento. O possÃvel mecanismo da A/G no processo estudado refere-se a processos mecÃnicos de interaÃÃo cÃlula-cÃlula (ZO-1 e ocludina) e/ou eletrolÃticos (claudina-2).
The prolonged and exhaustive exercise induces intestinal barrier dysfunction. Several studies show that supplementation with alanyl-glutamine (A/G) improves the cell proliferation intestinal and electrolyte absorption. The aim of our study was to investigate the effect of supplementation with A/G in the intestinal permeability in rats trained after prolonged exercise and exhaustive swimming. We used Wistar rats that were divided into seven groups: 1) Sedentary (S); 2) Sedentary A/G (S-A/G); 3) Trained (T); 4) Trained A/G (T-A/G); 5) Exhaustion (E); 6) Exhaustion A/G (E-A/G); 7) Recovered (R). The animal supplemented groups received the dipeptide A/G. The animals were trained for twelve weeks. In the methodology we performed biochemical analysis of pH, pCO2, pO2, SO2, and bases excess (BE), by the method of gas analysis and lactate and glucose. We analyzed the transcription of tight junctions: ZO-1, Occludin, Claudin-2 and PEPT-1 by RT-PCR. The analysis of intestinal permeability was performed by the method of the ingestion of lactulose/mannitol (L/M). We also performed histological analysis of the duodenum, jejunum and ileum. This study was approved by the CEPA-UFC on Protocol NÂ 13/2013. Our results showed that SO2 and pCO2 were higher in groups E and E-A/G, but decreased the parameters pH and BE for these same groups. We found falling glucose levels and increased concentrations of lactate. A significant increase in the percentage of excretion of lactulose in groups E and E-A/G than in group S. There was, however, fall of excretion of lactulose with statistical difference between groups E and E-A/G, showing protection against the alanyl-glutamine increased intestinal permeability promoted by exhaustive exercise. The percentage of excretion of mannitol was increased in groups E and E-A/G than in group S. However, in the analysis of the excretion of both carbohydrates lactulose/mannitol we observed a significant increase in group E than in group S. However, there was significant difference between groups E and E-A/G showing that Ala/Gln was able to reverse the effects of exhaustive activity in intestinal permeability. We observed an increase in ZO-1 and occludin in groups S-A/G and T with respect to S. There was also an increase of ZO-1 in the E group compared to S. However, Ala/Gln reversed the transcription of these tight junctions in groups T-A/G and E-A/G. Transcription of claudin-2 was reduced in the S-A/G, but we obtained and increase in the E group compared to a decrease of S and E-A/G against E. Regarding the PET-1 we showed increased transcription in groups T and E in relation to S. However, the Ala/Gln reversed the transcript of this dipeptide in group E-A/G with respect to E. An analysis 72 hours after the exhaustion test values found for intestinal permeability similar to sedentary group. The prolonged and exhaustive exercise altered intestinal permeability and chronic supplementation with Ala/Gln was protective against the increase. The possible mechanism of Ala/Gln refers to mechanical processes of cell-to-cell interaction (occludin and ZO-1) and/or electrolytic (claudin-2).