Document Detail

Prevention of hemorrhagic shock-induced intestinal tissue injury by glutamine via heme oxygenase-1 induction.
MedLine Citation:
PMID:  18497709     Owner:  NLM     Status:  MEDLINE    
Hemorrhagic shock (HS) is an oxidative stress that causes intestinal tissue injury. Heme oxygenase 1 (HO-1) is induced by oxidative stress and is thought to play an important role in the protection of tissues from oxidative injury. We previously reported the ileum to be the most susceptible to HS-induced tissue injury site in the intestine because HO-1 induction is the lowest at this site. We also previously demonstrated that glutamine (GLN) significantly induced HO-1 in the lower intestinal tract. In the present study, we investigated whether GLN pretreatment improves HS-induced intestinal tissue injury in the ileum by HO-1 induction. Treatment of rats with GLN (0.75 g/kg, i.v.) markedly induced functional HO-1 protein in mucosal epithelial cells in the ileum. Glutamine treatment before HS (MAP of 30 mmHg for 60 min) significantly ameliorated HS-induced mucosal inflammation and apoptotic cell death in the ileum, as judged by significant decreases in gene expression of TNF-alpha, iNOS, intercellular adhesion molecule 1, and vascular cell adhesion molecule 1, myeloperoxidase activity, the number of infiltrated neutrophils, DNA fragmentation by in situ oligo ligation assay, and activated caspase-3 expression, and by increases in gene expression of IL-10 and Bcl-2. In contrast, treatment with tin mesoporphyrin, a specific inhibitor of HO activity, abolished the beneficial effect of GLN pretreatment. These findings indicate that GLN pretreatment significantly ameliorated tissue injury in the ileum after HS by inducing HO-1. Glutamine treatment may thus protect mucosal cells from HS-induced oxidative damage via the anti-inflammatory and antiapoptotic properties of HO-1.
Kana Umeda; Toru Takahashi; Kazuyoshi Inoue; Hiroko Shimizu; Shigeru Maeda; Hiroshi Morimatsu; Emiko Omori; Reiko Akagi; Hiroshi Katayama; Kiyoshi Morita
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Shock (Augusta, Ga.)     Volume:  31     ISSN:  1540-0514     ISO Abbreviation:  Shock     Publication Date:  2009 Jan 
Date Detail:
Created Date:  2008-12-16     Completed Date:  2009-03-30     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9421564     Medline TA:  Shock     Country:  United States    
Other Details:
Languages:  eng     Pagination:  40-9     Citation Subset:  IM    
Department of Anesthesiology and Resuscitology, Okayama University Medical School, Okayama, Japan.
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MeSH Terms
Apoptosis / drug effects
Caspase 3 / biosynthesis
Enzyme Induction / drug effects
Enzyme Inhibitors / pharmacology
Glutamine / pharmacology*
Heme Oxygenase-1 / antagonists & inhibitors,  biosynthesis*
Ileal Diseases / enzymology,  pathology,  prevention & control
Ileum / enzymology,  pathology
Inflammation / enzymology,  pathology,  prevention & control
Intercellular Adhesion Molecule-1 / biosynthesis
Interleukin-10 / biosynthesis
Intestinal Mucosa / enzymology*,  injuries*,  pathology
Mesoporphyrins / pharmacology
Nitric Oxide Synthase Type II / biosynthesis
Oxidative Stress / drug effects
Proto-Oncogene Proteins c-bcl-2
Rats, Sprague-Dawley
Shock, Hemorrhagic / enzymology*,  pathology,  prevention & control*
Tumor Necrosis Factor-alpha / biosynthesis
Vascular Cell Adhesion Molecule-1 / biosynthesis
Reg. No./Substance:
0/Enzyme Inhibitors; 0/Mesoporphyrins; 0/Proto-Oncogene Proteins c-bcl-2; 0/Tumor Necrosis Factor-alpha; 0/Vascular Cell Adhesion Molecule-1; 126547-89-5/Intercellular Adhesion Molecule-1; 130068-27-8/Interleukin-10; 493-90-3/mesoporphyrin IX; 56-85-9/Glutamine; EC Oxide Synthase Type II; EC protein, rat; EC Oxygenase-1; EC 3.4.22.-/Casp3 protein, rat; EC 3.4.22.-/Caspase 3

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