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首页> 美国卫生研究院文献>Nutrients >Dietary Synbiotic Supplementation Protects Barrier Integrity of Hepatocytes and Liver Sinusoidal Endothelium in a Mouse Model of Chronic-Binge Ethanol Exposure
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Dietary Synbiotic Supplementation Protects Barrier Integrity of Hepatocytes and Liver Sinusoidal Endothelium in a Mouse Model of Chronic-Binge Ethanol Exposure

机译：饮食中的合生元补充剂可保护慢性宾果乙醇暴露小鼠模型中肝细胞和肝窦窦内皮的屏障完整性

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Alcohol overconsumption disrupts the gut microbiota and intestinal barrier, which decreases the production of beneficial microbial metabolic byproducts and allows for translocation of pathogenic bacterial-derived byproducts into the portal-hepatic circulation. As ethanol is known to damage liver sinusoidal endothelial cells (LSEC), here we evaluated dietary supplementation with a previously studied synbiotic on gut microbial composition, and hepatocyte and LSEC integrity in mice exposed to ethanol. We tested a chronic-binge ethanol feeding mouse model in which C57BL/6 female mice were fed ethanol (5% vol/vol) for 10 days and provided a single ethanol gavage (5 g/kg body weight) on day 11, 6 h before euthanasia. An ethanol-treatment group also received oral supplementation daily with a synbiotic; and an ethanol-control group received saline. Control mice were pair-fed and isocalorically substituted maltose dextran for ethanol over the entire exposure period; they received a saline gavage daily. Ethanol exposure decreased gut microbial abundance and diversity. This was linked with diminished expression of adherens junction proteins in hepatocytes and dysregulated expression of receptors for advanced glycation end-products; and this coincided with reduced expression of endothelial barrier proteins. Synbiotic supplementation mitigated these effects. These results demonstrate synbiotic supplementation, as a means to modulate ethanol-induced gut dysbiosis, is effective in attenuating injury to hepatocyte and liver endothelial barrier integrity, highlighting a link between the gut microbiome and early stages of acute liver injury in ethanol-exposed mice.
机译：过量饮酒会破坏肠道菌群和肠道屏障，从而减少有益微生物代谢副产物的产生，并使病原性细菌衍生副产物易位进入肝门肝循环。由于已知乙醇会损害肝正弦血管内皮细胞（LSEC），因此我们在这里评估了饮食中添加了先前研究的肠道微生物组成上的合生元，以及暴露于乙醇的小鼠的肝细胞和LSEC完整性。我们测试了一种慢性暴饮暴食的乙醇喂养小鼠模型，其中C57BL / 6雌性小鼠接受乙醇（5％vol / vol）喂养10天，并在第11天，第6小时提供一次单独的乙醇管饲（5 g / kg体重）安乐死之前。乙醇治疗组还每天口服一种合生元补充剂。乙醇对照组接受生理盐水。在整个暴露期间，对对照小鼠进行配对喂养，并用异麦芽酮糖替代了麦芽糖葡聚糖。他们每天接受盐水管饲。乙醇暴露会降低肠道微生物的丰度和多样性。这与肝细胞中粘附连接蛋白的表达减少和晚期糖基化终产物受体的表达失调有关。并且这与内皮屏障蛋白表达降低相吻合。合生元补充减轻了这些影响。这些结果表明，合生元补充作为调节乙醇诱导的肠道营养不良的一种手段，可有效减轻对肝细胞和肝内皮屏障完整性的损伤，突出了肠道微生物组与乙醇暴露小鼠急性肝损伤早期之间的联系。

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