title: Taurine attenuates multiple organ injury induced by intestinal ischemia reperfusion in rats.
abstract: BACKGROUND
  Intestinal ischemia reperfusion (II/R) is a serious clinical condition associated with simultaneous multiple organ dysfunction. The purpose of this study was to investigate whether taurine, an anti-oxidative, anti-inflammatory, and anti-apoptotic agent, could attenuate multiple organ injury induced by II/R.
  
  
  METHODS
  Taurine was intravenously injected to Wistar rats 30 min before II/R; physiological saline and sham operation served as controls. II/R was produced by occlusion of superior mesenteric artery for 60 min. Rats were randomly sacrificed 1.5, 3, 12, and 36 h after II/R; blood samples were collected for assessing alanine aminotransferase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN), creatinine (Cr), and tumor necrosis factor-alpha (TNF-alpha), and intestines, livers, kidneys, and lungs were removed for histological examination of scoring injury severity and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling analysis. The amount of lipid peroxides (LPO) was measured in intestinal tissues, and expression of caspase-3 was detected in all of the tissues with Western blot analysis.
  
  
  RESULTS
  II/R resulted in injury to intestines as well as livers, kidneys, and lungs, evidenced by morphological alteration, increased cell apoptosis, and elevated serum levels of ALT, AST, BUN, and Cr. The damage reached peak 3 h after II/R. The intestinal LPO and serum levels of TNF-alpha were increased after II/R. Pre-administration of taurine significantly attenuated multiple organ injury as the histological score, apoptosis index, LPO, and levels of ALT, AST, BUN, Cr, and TNF-alpha were significantly lower compared with saline controls.
  
  
  CONCLUSIONS
  Taurine attenuates multiple organ injury induced by II/R. Although the mechanism needs further investigation, taurine inhibits production of intestinal LPO, release of TNF-alpha, cell apoptosis, and expression of caspase-3.
authors.affiliation: Department of General Surgery, The Fifth Affiliated Hospital of Harbin Medical University, Daqing, China.
authors.forename: Feng
authors.initials: F
authors.lastname: Zhang
authors.forename: Liquan
authors.initials: L
authors.lastname: Tong
authors.forename: Haiquan
authors.initials: H
authors.lastname: Qiao
authors.forename: Xuesong
authors.initials: X
authors.lastname: Dong
authors.forename: Guojun
authors.initials: G
authors.lastname: Qiao
authors.forename: Hongchi
authors.initials: H
authors.lastname: Jiang
authors.forename: Xueying
authors.initials: X
authors.lastname: Sun
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage* / Q000494:pharmacology; D000975:Antioxidants / Q000008:administration & dosage* / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects; D004195:Disease Models, Animal; D007275:Injections, Intravenous; D007410:Intestinal Diseases / Q000150:complications*; D007422:Intestines / Q000098:blood supply; D008297:Male; D009102:Multiple Organ Failure / Q000209:etiology / Q000517:prevention & control*; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000150:complications*; D013654:Taurine / Q000008:administration & dosage* / Q000494:pharmacology
chemical_list: D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D013654:Taurine