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首页> 外文期刊>Alcohol >Ethanol increases tumor necrosis factor-alpha receptor-1 (TNF-R1) levels in hepatic, intestinal, and cardiac cells.
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Ethanol increases tumor necrosis factor-alpha receptor-1 (TNF-R1) levels in hepatic, intestinal, and cardiac cells.

机译：乙醇会增加肝，肠和心脏细胞中的肿瘤坏死因子-α受体1（TNF-R1）水平。

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Abstract Chronic ethanol consumption leads to cell injury in virtually every tissue. Tumor necrosis factor-alpha (TNF-alpha) constitutes a major factor in the development of alcohol-induced liver injury. In alcohol-dependent subjects, elevated levels of plasma TNF-alpha are strongly predictive of mortality. Binding of TNF-alpha to TNF-alpha receptor-1 (TNF-R1) activates death domain pathways, leading to necrosis and apoptosis in most tissues, and it also increases the expression of intercellular adhesion molecules (i.e., ICAM-1), which promote inflammation. We determined whether ethanol exposure leads to increases in cellular TNF-R1. We incubated HepG2 human hepatoma cells and H4-II-E-C3 rat hepatoma cells with 25, 50, and 100 mM ethanol for various intervals of time up to 48 h. Human colonic adenocarcinoma cells (Caco-2 cells) and neonatal rat primary cardiomyocytes were also incubated with different concentrations of ethanol. Levels of TNF-R1 were measured either by a sandwich enzyme-linked immunosorbent assay (ELISA) method or by determining the extracellular transmembrane domain of TNF-R1 by an intact-cell ELISA method. Ethanol exposure for 48 h increased TNF-R1 levels in human hepatoma cells in a dose-dependent manner. Levels increased significantly by 164% at 50 mM and by 240% at 100 mM ethanol. Effects were time dependent and did not reach a plateau at 48 h. Similar increases in TNF-R1 were also observed in rat hepatoma cells (90% at 50 mM and 230% at 100 mM ethanol). Under similar conditions, Caco-2 cells showed a significant 80% increase in TNF-R1 levels at 200 mM ethanol, a concentration found in intestine. Neonatal rat primary cardiomyocytes showed TNF-R1 increases of 36% at 50 mM and 44% at 100 mM ethanol. These results indicate that exposure of different cell types to pharmacologic concentrations of ethanol increases TNF-R1 levels and may augment TNF-alpha-mediated cell injury in different tissues.
机译：摘要慢性乙醇的消耗实际上会导致每个组织的细胞损伤。肿瘤坏死因子-α（TNF-α）构成酒精诱导的肝损伤发展的主要因素。在酒精依赖的受试者中，血浆TNF-α水平的升高强烈预示了死亡率。 TNF-α与TNF-α受体1（TNF-R1）的结合激活了死亡域途径，导致大多数组织中的坏死和凋亡，并且还增加了细胞间粘附分子（ICAM-1）的表达，促进炎症。我们确定乙醇暴露是否导致细胞TNF-R1增加。我们将HepG2人肝癌细胞和H4-II-E-C3大鼠肝癌细胞与25、50和100 mM乙醇孵育长达48小时的各种时间间隔。还用不同浓度的乙醇孵育人结肠腺癌细胞（Caco-2细胞）和新生大鼠原代心肌细胞。通过夹心酶联免疫吸附测定（ELISA）方法或通过完整细胞ELISA方法确定TNF-R1的细胞外跨膜结构域来测量TNF-R1的水平。乙醇暴露48 h以剂量依赖性方式增加人肝癌细胞中TNF-R1的水平。在50 mM时，水平显着增加164％，在100 mM乙醇中，水平显着增加240％。效果是时间依赖性的，并且在48小时内未达到平稳状态。在大鼠肝癌细胞中也观察到了类似的TNF-R1升高（在50 mM时为90％，在100 mM乙醇时为230％）。在相似的条件下，Caco-2细胞在200 mM乙醇（肠中发现的浓度）下显示TNF-R1水平显着增加80％。新生大鼠原代心肌细胞显示TNF-R1在50 mM时增加36％，在100 mM乙醇时增加44％。这些结果表明，不同细胞类型暴露于药理浓度的乙醇会增加TNF-R1水平，并可能加剧不同组织中TNF-α介导的细胞损伤。

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