title: Glycine reduces hepatic warm ischaemia-reperfusion injury by suppressing inflammatory reactions in rats.
abstract: BACKGROUND
  Glycine, a non-essential amino acid, is known to have an anti-inflammatory effect on haemorrhagic and endotoxic shock in animals. In the present study, we examined the effects of glycine on inflammatory reactions and hepatocellular damage after hepatic warm ischaemia-reperfusion (I-R) in rats.
  
  
  METHODS
  Using Sprague-Dawley rats, ischaemia was induced in 92% of the liver by clamping the hepatic inflows for 60 min, and part of the non-ischaemic lobe was resected after reperfusion. Before the induction of I-R, rats were treated by an intravenous administration of either glycine (Glycine group) or normal saline (Control group). The severity of hepatocellular injury was determined by serum levels of hepatic enzymes and histological necrosis. To evaluate the effect of glycine on inflammatory reactions, tumour necrosis factor (TNF)-alpha mRNA expression in the liver, serum levels of TNF-alpha and chemokine-induced neutrophil chemoattractant (CINC) and the number of neutrophils in the liver were compared between the groups.
  
  
  RESULTS
  At 60 min after reperfusion, the serum levels of hepatic enzymes in the Glycine group were significantly lower than those in the Control group (P<0.05). TNF-alpha mRNA expression was also suppressed in the livers in the Glycine group. Furthermore, the serum levels of TNF-alpha and CINC in the Glycine group were significantly lower than those in the Control group (P<0.05). Pretreatment with glycine also significantly reduced hepatic necrosis and the number of neutrophils at 24 h after reperfusion.
  
  
  CONCLUSIONS
  Glycine has a protective effect against inflammatory reactions, and reduces hepatocellular injury induced by hepatic warm I-R in rats.
authors.affiliation: Department of Liver Transplantation and Digestive Surgery, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan. ymanouch@gk9.so-net.ne.jp
authors.forename: Kosho
authors.initials: K
authors.lastname: Yamanouchi
authors.forename: Susumu
authors.initials: S
authors.lastname: Eguchi
authors.forename: Yukio
authors.initials: Y
authors.lastname: Kamohara
authors.forename: Katsuhiko
authors.initials: K
authors.lastname: Yanaga
authors.forename: Sadayuki
authors.initials: S
authors.lastname: Okudaira
authors.forename: Yoshitsugu
authors.initials: Y
authors.lastname: Tajima
authors.forename: Takashi
authors.initials: T
authors.lastname: Kanematsu
mesh_terms: D000410:Alanine Transaminase / Q000378:metabolism; D000818:Animals; D054360:Chemokine CXCL1 / Q000378:metabolism; D005998:Glycine / Q000627:therapeutic use*; D018684:Glycine Agents / Q000627:therapeutic use*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D015227:Lipid Peroxidation; D008099:Liver / Q000187:drug effects* / Q000201:enzymology / Q000293:injuries; D008297:Male; D009336:Necrosis; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000378:metabolism / Q000517:prevention & control*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism; D052096:Warm Ischemia
chemical_list: D054360:Chemokine CXCL1; C513297:Cxcl1 protein, rat; D018684:Glycine Agents; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D007770:L-Lactate Dehydrogenase; D000410:Alanine Transaminase; D005998:Glycine