title: Tissue-protective effect of glutamine on hepatic ischemia-reperfusion injury via induction of heme oxygenase-1.
abstract: OBJECTIVE
  Glutamine showed cytoprotective activity in vitro on anoxia-reoxygenation injury via induction of heme oxygenase-1 (HO-1). We thus investigated its in vivo tissue-protective effect in a rat liver ischemia-reperfusion (I/R) model.
  
  
  METHODS
  Before the I/R procedure, animals were treated with glutamine. Liver injury was evaluated by serum liver enzymes, histological examination and apoptosis detection by transferase-mediated uridine nick end labeling staining. Meanwhile, expression and activities of HO-1 were measured by Western blot and a biochemical method. Liver blood flow was measured by using a laser Doppler flowmeter, and oxidative injury was investigated by the thiobarbituric acid-reactive substance (TBARS) assay. The inflammatory cytokine monocyte chemotactic protein (MCP)-1 was quantified by ELISA.
  
  
  RESULTS
  I/R caused a large increase in levels of liver enzymes, remarkably inducing the necrosis and apoptosis of liver tissue, which was markedly inhibited by glutamine, during which HO-1 was upregulated significantly, and the HO-1 inhibitor zinc protoporphyrin nullified the effect of glutamine. Liver blood flow was greatly reduced after I/R; however, it was significantly improved by glutamine. Lipid peroxidation (TBARS) in liver tissue was largely induced which was significantly lowered by glutamine. Similar results were also observed for the production of MCP-1.
  
  
  CONCLUSIONS
  Glutamine protected tissue against oxidative injury during rat hepatic I/R, by induction of HO-1 to fulfill antioxidative and antiapoptotic effects.
authors.affiliation: School of Public Health, Anhui Medical University, Hefei City, China.
authors.forename: Shi-Chen
authors.initials: SC
authors.lastname: Zhang
authors.forename: Qiang
authors.initials: Q
authors.lastname: Shi
authors.forename: Ya-Ni
authors.initials: YN
authors.lastname: Feng
authors.forename: Jun
authors.initials: J
authors.lastname: Fang
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D018932:Chemokine CCL2 / Q000097:blood; D005973:Glutamine / Q000494:pharmacology / Q000627:therapeutic use*; D006419:Heme Oxygenase (Decyclizing) / Q000378:metabolism*; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008099:Liver / Q000098:blood supply / Q000187:drug effects / Q000378:metabolism; D008107:Liver Diseases / Q000188:drug therapy* / Q000378:metabolism; D008297:Male; D020011:Protective Agents / Q000494:pharmacology / Q000627:therapeutic use*; D051381:Rats; D017208:Rats, Wistar; D012039:Regional Blood Flow / Q000187:drug effects; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: C491766:Ccl2 protein, rat; D018932:Chemokine CCL2; D020011:Protective Agents; D017392:Thiobarbituric Acid Reactive Substances; D005973:Glutamine; D007770:L-Lactate Dehydrogenase; D006419:Heme Oxygenase (Decyclizing); C491523:Hmox1 protein, rat; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase