ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2013
Lipopolysaccharide-induced failure of the gut barrier is site-specific and inhibitable by growth hormone.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 27 citations in OpenAlex.
- Gut alterations in a chronic kidney disease rat model with diet-induced vascular calcification.FEBS open bio · 2025Article
- Preventing Bacterial Translocation in Patients with Leaky Gut Syndrome: Nutrition and Pharmacological Treatment Options.International journal of molecular sciences · 2022Review
- GLP-2 Acutely Prevents Endotoxin-Related Increased Intestinal Paracellular Permeability in Rats.Digestive diseases and sciences · 2020Article
- Article
- Tissue-Specific GHR Knockout Mice: An Updated Review.Frontiers in endocrinology · 2020Review
- Animal Models of Undernutrition and Enteropathy as Tools for Assessment of Nutritional Intervention.Nutrients · 2019Review
- Propofol Does Not Reduce Pyroptosis of Enterocytes and Intestinal Epithelial Injury After Lipopolysaccharide Challenge.Digestive diseases and sciences · 2018Article
- Growth Hormone Resistance-Special Focus on Inflammatory Bowel Disease.International journal of molecular sciences · 2017Review
- Severity of pancreatitis‑associated intestinal mucosal barrier injury is reduced following treatment with the NADPH oxidase inhibitor apocynin.Molecular medicine reports · 2016Article
- Ginsenoside Rb1 protects the intestinal mucosal barrier following peritoneal air exposure.Experimental and therapeutic medicine · 2016Article
- HIV-1 Tat exacerbates lipopolysaccharide-induced cytokine release via TLR4 signaling in the enteric nervous system.Scientific reports · 2016Article
- Chronic Kidney Disease Induced Intestinal Mucosal Barrier Damage Associated with Intestinal Oxidative Stress Injury.Gastroenterology research and practice · 2016Article
- The Endoplasmic Reticulum Stress Sensor IRE1α in Intestinal Epithelial Cells Is Essential for Protecting against Colitis.The Journal of biological chemistry · 2015Article
- Therapeutic effect of Qingyi decoction in severe acute pancreatitis-induced intestinal barrier injury.World journal of gastroenterology · 2015Article
- The effect of peritoneal air exposure on intestinal mucosal barrier.Gastroenterology research and practice · 2014Article
- Characterization of an intestine-specific GH receptor knockout (IntGHRKO) mouse.Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research SocietyArticle
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8 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundGut barrier failure caused by endotoxemia is a life-threatening problem. The present study aimed to determine whether any specific intestinal site is highly correlated with gut barrier failure, and whether recombinant human growth hormone (rhGH) can ameliorate gut barrier failure in a rat model of endotoxemia.
methodsEnterostomy tubes were surgically placed in adult male Sprague-Dawley rats three days before induction of endotoxemia by lipopolysaccharide (LPS) injection. Controls received no LPS. Rats were then randomly assigned to receive subcutaneous injections of rhGH (experimental, n = 30) or 0.9 % saline (control, n = 15) at 24, 48, or 72 h after LPS injection. Escherichia coli labeled with green fluorescent protein (GFP) were injected into the intestinal segment of all rats through the enterostomy tubes. The number of GFP-labeled E. coli detected in mesenteric lymph nodes was examined after 96 h. Apoptosis and proliferation rates of intestinal epithelial cells, and intestinal permeability were measured.
resultsEndotoxemia led to high mortality, compared with the control group, and rhGH treatment did not improve survival. Intestinal permeability, reflected by translocation rates of GFP-labeled E. coli, and apoptosis rates in the LPS-induced endotoxemia group were higher than those in the non-endotoxemia control group, and the endotoxemia ileum group had the highest rates of both bacterial translocation and apoptosis. The LPS+GH group had less bacterial translocation and apoptosis than the LPS-induced endotoxemia group. In contrast, the proliferation rates were lower in the LPS group compared to the LPS+GH group.
conclusionsEndotoxemia can induce gut barrier failure in rats, and the ileum is the site of greatest risk. The GH can reduce the incidence of endotoxemia-induced gut barrier failure, but not the associated mortality.
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