Membrane peroxidation by lipopolysaccharide and iron-ascorbate adversely affects Caco-2 cell function: beneficial role of butyric acid

Courtois, Frédéric; Seidman, Ernest G.; Delvin, Edgard; Asselin, Claude; Bernotti, Sandra; Ledoux, M.; Lévy, Émile

doi:10.1093/ajcn/77.3.744

Cited by 43 publications

(37 citation statements)

References 38 publications

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“…In addition, treatment of hamsters with TNF or IL-1 produced a reduction in hepatic mRNA levels of SR-BI. Previous studies have documented the participation of TNF-a and LPS in the disturbance of lipid metabolism in the gastrointestinal tract and blood circulation Murthy et al, 1996Murthy et al, , 2000Dube et al, 2001;Bernotti et al, 2003;Courtois et al, 2003;Levy et al, 2003]. The results of our study confirm these in vitro observations and demonstrate for the first time the downregulation of SR-BI protein expression by basolateral TNF-a, apical IFN-g and LPS on both sides.…”

Section: Discussionsupporting

confidence: 90%

Asymmetrical regulation of scavenger receptor class B type I by apical and basolateral stimuli using Caco‐2 cells

Peretti

Delvin

Sinnett

et al. 2006

J of Cellular Biochemistry

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Cholesterol uptake and the mechanisms that regulate cholesterol translocation from the intestinal lumen into enterocytes remain for the most part unclear. Since scavenger receptor class B type I (SR-BI) has been suggested to play a role in cholesterol absorption, we investigated cellular SR-BI modulation by various potential effectors administered in both apical and basolateral sides of Caco-2 cells. With differentiation, Caco-2 cells increased SR-BI protein expression. Western blot analysis showed the ability of cholesterol and oxysterols in both cell compartments to reduce SR-BI protein expression. Among the n-3, n-6, and n-9 fatty acid families, only eicosapentaenoic acid was able to lower SR-BI protein expression on both sides, whereas apical alpha-linolenic acid decreased SR-BI abundance and basolateral arachidonic acid (AA) raised it. Epidermal growth factor and growth hormone, either in the apical or basolateral medium, diminished SR-BI cellular content, while insulin displayed the same effect only on the basolateral side. In the presence of proinflammatory agents (LPS, TNF-alpha, IFN-gamma), Caco-2 cells exhibited differential behavior. SR-BI was downregulated by lipopolysaccharide on both sides. Finally, WY-14643 fibrate diminished SR-BI protein expression when it was added to the apical medium. Biotinylation studies in response to selected stimuli revealed that regulatory modifications in SR-BI protein expression occurred for the most part at the apical cell surface irrespective of the effector location. Our data indicate that various effectors supplied to the apical and basolateral compartments may impact on SR-BI at the apical membrane, thus suggesting potential regulation of intestinal cholesterol absorption and distribution in various intracellular pools.

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Section: Discussionsupporting

confidence: 90%

Asymmetrical regulation of scavenger receptor class B type I by apical and basolateral stimuli using Caco‐2 cells

Peretti

Delvin

Sinnett

et al. 2006

J of Cellular Biochemistry

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“…Iron ascorbate was prepared as previously described. 19) When filter-grown cells were treated with the chemicals described above, the culture medium was changed on the apical and/or basolateral side. Cell viability was assessed by counting cells attached to the filter at 24 h after treatment.…”

Section: Methodsmentioning

confidence: 99%

Prevention of Barrier Disruption by Heme Oxygenase-1 in Intestinal Bleeding Model

Akagi

Hatori

et al. 2016

Biological & Pharmaceutical Bulletin

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In this study we investigated the effect of free heme, the local level of which was increased by bleeding, on the intestinal barrier function, using human epithelial colorectal adenocarcinoma cells (Caco-2). Our results show that the addition of hemin to the culture medium markedly disrupted the barrier function, which was significantly improved by glutamine supplementation. Although hemin treatment caused the increased expression of heme oxygenase (HO)-1, the inhibition of HO activity resulted in the aggravation of hemin-induced barrier dysfunction. Up-regulation of HO-1 by pretreatment with a low concentration of hemin almost completely prevented hemin-induced barrier dysfunction. Taken together, these observations indicate that an abnormally high level of intracellular free heme causes barrier dysfunction, probably through the modulation of proteins forming tight junctions.

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“…Идея моделирования свободно радикального повреждения легких in vivo была заим ствована из метода индукции образования АФК, описанного для применения in vitro [9,10]. В основе лежит общеизвестная реакция Фентона (1, 2) и спо собность аскорбата восстанавливать железо с обра зованием Fe 2 + (3) [12]: Возможность коррекции изменений в легких, развивающихся вследствие гипероксии, изучалась с помощью ингаляционного введения антиоксидан тов: 20% ного раствора для ингаляций N ацетилци стеина (NAC) (Белмедпрепараты, Беларусь), α то коферола, all trans ретинола, all trans ретиноевой кислоты (Sigma, США).…”

Section: материалы и методыunclassified

“…Данная смесь неоднократно применялась в экспериментах на различных типах клеток в каче стве индуктора генерации свободных радикалов [9,10], однако по имеющимся данным, in vivo для сти муляции повреждения легких ранее не использова лась. В настоящем исследовании изменения, выяв ленные в легких при эксперименте, моделирующем индукцию АФК in vivo с использованием системы Fe 2+ -аскорбат, оказались весьма сходны с теми, ко торые были описаны ранее при гипероксии (по дан ным литературы) [6,7].…”

Section: результаты и обсуждениеunclassified

Morphological basis of lung injury by free radicals and the treatment in newborn guinea pigs

Таганович¹,

Anishchenko²,

Kotovich³

et al. 2013

Pulʹmonologiâ (Mosk.)

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Morphological basis of lung injury by free radicals and the treatment in newborn guinea pigs SummaryStructural and morphometrical lung changes in guinea pigs exposed to hyperoxia or induced reactive oxygen species (ROS) production during 14 days alone or under inhalations of N acetylcysteine (in water solution or built in multilayered liposomes), α tocopherol or retinol have been stud ied. We established that induced ROS production in the lungs was associated with structural change of the lung tissue compatible with that in ani mals exposed to hyperoxia. Most typical changes associated with hyperoxia and induced ROS production were reduction in the alveolar intercept area and increase in the total area of the alveolar space and intrapulmonary vessel lumen. All the therapy regimens effectively prevented hyperoxia induced changes of the alveolar space / interstitium relationship but were fail to prevent the dilation of the intrapulmonary vessels. The inhalation of N acetylcysteine seemed to be the most effective treatment.

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Membrane peroxidation by lipopolysaccharide and iron-ascorbate adversely affects Caco-2 cell function: beneficial role of butyric acid

Abstract: Bacterial endotoxin and prooxidants may overwhelm antioxidant defenses and become deleterious to enterocyte function, whereas butyric acid and BHT may provide antioxidant protection.

Cited by 43 publications

References 38 publications

Asymmetrical regulation of scavenger receptor class B type I by apical and basolateral stimuli using Caco‐2 cells

Asymmetrical regulation of scavenger receptor class B type I by apical and basolateral stimuli using Caco‐2 cells

Prevention of Barrier Disruption by Heme Oxygenase-1 in Intestinal Bleeding Model

Morphological basis of lung injury by free radicals and the treatment in newborn guinea pigs

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