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cells, mice, nox, epithelial, colonic, propionate, pubmed, article, fig, expression, intestinal, google, scholar, liver, hdac, injury, ncm, cas, stress, ros, oxidative, analysis, levels, group, histone, compared, gut, apoptosis, tnfα, colon, staining, barrier, showed, groups, chronicbinge, ethanolfed, ffar, nadph, ethanol, central, gene, proteins, protein, control, cell, increased, disease, acetylation, decreased, treated,

Topics {✒️}

chronic–binge ethanol-fed mice chronic–binge alcohol-exposed mice lipopolysaccharide-induced il-1β expression ethanol-induced liver injury alcohol-induced liver injury ethanol-induced fatty liver alcohol-caused liver injury alcohol-induced liver disease alcohol-induced gut leakiness alcohol-related ros injury diet-induced protein oxidation alcohol-related liver disease redox-sensitive nf-κb tnf-α-treated ncm460 cells short-chain fatty acids chronic alcohol-exposed mice gut-derived microbial products ultra-sensitive ecl reagents prevent alcohol-related apoptosis cardiac ischemia-reperfusion injury nox1-mediated oxidative stress alcohol-exposed caco-2 cells anti-rna polymerase ii alcohol-induced nox1 expression article download pdf tnf-α caused apoptosis binge ethanol feeding ethanol-exposed mice treated ubiquitin-dependent proteolytic degradation ethanol-fed mice compared ethanol-exposed mice compared alcohol-exposed mice compared oct-embedded liver tissues chronic ethanol diet histone deacetylase-dependent mechanisms nadph-stimulated ros formation chronic alcohol exposure amp-activated protein kinase chronic dss colitis quantitative real-time pcr tnf-α-treated ncm460 oxidative stress injury 250 mg/kg body weight cellular component classification tnf-α induced chronic ethanol consumption intestinal barrier injury intestinal oxidative injury randomized placebo-controlled study alcoholic liver disease

Questions {❓}

• The intestinal epithelial barrier: a therapeutic target?

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         headline:The role of NADPH oxidase 1 in alcohol-induced oxidative stress injury of intestinal epithelial cells
         description:Alcohol-mediated reactive oxygen species (ROS) play a vital role in intestinal barrier injury. However, the mechanism of ROS accumulation in enterocytes needs to be explored further. In our study, we found that chronic–binge ethanol-fed mice had increased levels of gut oxidative stress and high intestinal permeability. The transcription profiles of the colonic epithelial cells showed that the level of NADPH oxidase 1 (NOX1) was significantly elevated in alcohol-exposed mice compared with isocaloric-exposed mice. In vitro, NOX1 silencing alleviated ROS accumulation and the apoptosis of human colonic epithelial cells (NCM460), while NOX1 overexpression accelerated oxidative stress injury of NCM460 cells. Propionic acid was reduced in the gut of chronic–binge ethanol-fed mice, compared with isocaloric-fed mice, as observed through untargeted metabolomic analysis. Supplementation with propionate relieved ethanol-induced liver and intestinal barrier injuries and reduced the level of ROS accumulation and apoptosis of ethanol-induced colonic epithelial cells. Propionate alleviating NOX1 induced ROS injury of colonic epithelial cells, independent of G protein-coupled receptors. Propionate significantly inhibited histone deacetylase 2 (HDAC2) expressions both in ethanol-exposed colonic epithelial cells and TNF-α-treated NCM460. Chromatin immunoprecipitation (ChIP) assays showed that propionate suppressed the NOX1 expression by regulating histone acetylation in the gene promoter region. In conclusion, NOX1 induces oxidative stress injury of colonic epithelial cells in alcohol-related liver disease. Propionate, which can act as an endogenous HDAC2 inhibitor, can decrease levels of apoptosis of intestinal epithelial cells caused by oxidative stress.
         datePublished:2022-05-31T00:00:00Z
         dateModified:2022-06-17T00:00:00Z
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            Alcoholic liver disease
            Propionate
            Apoptosis
            Colonic epithelial cells
            NADPH oxidase 1
            Cell Biology
            Pharmacology/Toxicology
            Biochemistry
            general
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      headline:The role of NADPH oxidase 1 in alcohol-induced oxidative stress injury of intestinal epithelial cells
      description:Alcohol-mediated reactive oxygen species (ROS) play a vital role in intestinal barrier injury. However, the mechanism of ROS accumulation in enterocytes needs to be explored further. In our study, we found that chronic–binge ethanol-fed mice had increased levels of gut oxidative stress and high intestinal permeability. The transcription profiles of the colonic epithelial cells showed that the level of NADPH oxidase 1 (NOX1) was significantly elevated in alcohol-exposed mice compared with isocaloric-exposed mice. In vitro, NOX1 silencing alleviated ROS accumulation and the apoptosis of human colonic epithelial cells (NCM460), while NOX1 overexpression accelerated oxidative stress injury of NCM460 cells. Propionic acid was reduced in the gut of chronic–binge ethanol-fed mice, compared with isocaloric-fed mice, as observed through untargeted metabolomic analysis. Supplementation with propionate relieved ethanol-induced liver and intestinal barrier injuries and reduced the level of ROS accumulation and apoptosis of ethanol-induced colonic epithelial cells. Propionate alleviating NOX1 induced ROS injury of colonic epithelial cells, independent of G protein-coupled receptors. Propionate significantly inhibited histone deacetylase 2 (HDAC2) expressions both in ethanol-exposed colonic epithelial cells and TNF-α-treated NCM460. Chromatin immunoprecipitation (ChIP) assays showed that propionate suppressed the NOX1 expression by regulating histone acetylation in the gene promoter region. In conclusion, NOX1 induces oxidative stress injury of colonic epithelial cells in alcohol-related liver disease. Propionate, which can act as an endogenous HDAC2 inhibitor, can decrease levels of apoptosis of intestinal epithelial cells caused by oxidative stress.
      datePublished:2022-05-31T00:00:00Z
      dateModified:2022-06-17T00:00:00Z
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         Alcoholic liver disease
         Propionate
         Apoptosis
         Colonic epithelial cells
         NADPH oxidase 1
         Cell Biology
         Pharmacology/Toxicology
         Biochemistry
         general
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      name:Division of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
      name:Division of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
      name:Division of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
      name:Division of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China

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