title: Oral arginine reduces gut mucosal injury caused by lipopolysaccharide endotoxemia in rat.
abstract: BACKGROUND
  The objective of this study was to evaluate the effects of lipopolysaccharide (LPS) endotoxemia and enteral arginine (ARG) supplementation on intestinal structural changes, enterocyte proliferation, and apoptosis in rat.
  
  
  METHODS
  Male Sprague-Dawley rats, weighing 250-280 g, were divided into three experimental groups: control rats, LPS rats treated with lipopolysaccharide given ip at a dose of 10 mg/kg every 24 h (two injections), and LPS-ARG rats treated with enteral arginine given in drinking water (2%) 72 h before and following injection of LPS. Intestinal structural changes, enterocyte proliferation, and enterocyte apoptosis were determined on day 3 following the first LPS injection.
  
  
  RESULTS
  LPS rats demonstrated a significant decrease in bowel weight in duodenum, mucosal weight in duodenum, jejunum, and ileum, mucosal DNA and protein in jejunum and ileum, and villus height in jejunum and ileum compared to control animals. LPS rats also had a significantly lower cell proliferation index in jejunum and ileum and a higher apoptotic index in jejunum and ileum compared to control rats. LPS-ARG animals demonstrated greater duodenal bowel weight, duodenal and ileal mucosal weight, ileal mucosal DNA and protein, ileal villus height, and jejunal and ileal cell proliferation index compared to LPS animals.
  
  
  CONCLUSIONS
  LPS endotoxemia impairs the integrity of the gastrointestinal mucosa in rat. Decreased cell proliferation and increased apoptosis may be considered the main mechanisms responsible for the decreased cell mass. Enteral arginine administration decreases the mucosal injury caused by lipopolysaccharide.
authors.affiliation: Rappaport Faculty of Medicine, Technion, Bnai Zion Medical Center, Haifa, Israel. igor-dr@internet-zahav.net
authors.forename: Igor
authors.initials: I
authors.lastname: Sukhotnik
authors.forename: Jorge
authors.initials: J
authors.lastname: Mogilner
authors.forename: Michael M
authors.initials: MM
authors.lastname: Krausz
authors.forename: Michael
authors.initials: M
authors.lastname: Lurie
authors.forename: Mark
authors.initials: M
authors.lastname: Hirsh
authors.forename: Arnold G
authors.initials: AG
authors.lastname: Coran
authors.forename: Eitan
authors.initials: E
authors.lastname: Shiloni
mesh_terms: D000284:Administration, Oral; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D001120:Arginine / Q000008:administration & dosage* / Q000494:pharmacology; D001835:Body Weight; D002455:Cell Division / Q000187:drug effects; D004247:DNA / Q000378:metabolism; D019446:Endotoxemia / Q000139:chemically induced / Q000401:mortality / Q000473:pathology* / Q000503:physiopathology; D007274:Injections, Intraperitoneal; D007413:Intestinal Mucosa / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology*; D007421:Intestine, Small / Q000473:pathology; D008070:Lipopolysaccharides / Q000008:administration & dosage; D008297:Male; D011506:Proteins / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D008070:Lipopolysaccharides; D011506:Proteins; D004247:DNA; D001120:Arginine