title: Hydrogen sulfide protects from intestinal ischaemia-reperfusion injury in rats.
abstract: OBJECTIVE
  Hydrogen sulfide (H2S) is an endogenously gaseous mediator, regulating many pathophysiological functions in mammalian cells. H2S has been shown to inhibit myocardial ischaemia-reperfusion (I/R) injury. However, little is known about whether H2S could modulate intestinal I/R injury. This study aimed to investigate the effect of H2S on intestinal I/R injury and potential mechanism(s) underlying the action of H2S in regulating the development of intestinal I/R injury in rats.
  
  
  METHODS
  Following surgical induction of intestinal I/R injury for 1 h, groups of Sprague-Dawley rats were treated with, or without, tetramethylpyrazine (8 mg/kg), or sodium hydrosulfide (NaHS, an H2S donor at 7 or 14 micromol/kg) 30 min after occlusion. All rats were sacrificed immediately after the reperfusion. Their intestinal injury, together with that of sham-control rats, was histologically examined and their sera and intestinal malondialdehyde (MDA), superoxide dismutase (SOD), peroxidase (GSH-Px) activities were characterized by biochemical analysis.
  
  
  RESULTS
  The results showed that NaHS significantly reduced intestinal I/R injury and the levels of sera and intestinal MDA activity, and dramatically increased the levels of serum and intestinal SOD and GSH-Px activity.
  
  
  CONCLUSIONS
  The results suggest that H2S protects from intestinal I/R injury in rats, which is associated with increase in the activity of antioxidant enzymes.
authors.affiliation: Department of General Surgery, the First Affiliated Hospital, Xi'an Jiaotong University College of Medicine, Xi'an, Shaanxi, P.R. China.
authors.forename: Hao
authors.initials: H
authors.lastname: Liu
authors.forename: Xiao-Bin
authors.initials: XB
authors.lastname: Bai
authors.forename: Song
authors.initials: S
authors.lastname: Shi
authors.forename: Yong-Xiao
authors.initials: YX
authors.lastname: Cao
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism / Q000627:therapeutic use; D004195:Disease Models, Animal; D005979:Glutathione Peroxidase / Q000096:biosynthesis / Q000187:drug effects / Q000627:therapeutic use; D006862:Hydrogen Sulfide / Q000737:chemistry / Q000494:pharmacology / Q000627:therapeutic use*; D007410:Intestinal Diseases / Q000150:complications / Q000517:prevention & control*; D008297:Male; D008315:Malondialdehyde / Q000037:antagonists & inhibitors / Q000097:blood / Q000737:chemistry; D008641:Mesenteric Vascular Occlusion / Q000150:complications / Q000503:physiopathology; D051381:Rats; D015427:Reperfusion Injury / Q000150:complications / Q000517:prevention & control*; D013440:Sulfides / Q000494:pharmacology / Q000627:therapeutic use; D013482:Superoxide Dismutase / Q000096:biosynthesis / Q000187:drug effects
chemical_list: D000975:Antioxidants; D013440:Sulfides; D008315:Malondialdehyde; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; C025451:sodium bisulfide; D006862:Hydrogen Sulfide