
Hydrogen sulfide protects from intestinal ischaemia–reperfusion injury in rats
Author(s) -
Liu Hao,
Bai XiaoBin,
Shi Song,
Cao YongXiao
Publication year - 2009
Publication title -
journal of pharmacy and pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 118
eISSN - 2042-7158
pISSN - 0022-3573
DOI - 10.1211/jpp.61.02.0010
Subject(s) - sodium hydrosulfide , malondialdehyde , superoxide dismutase , reperfusion injury , tetramethylpyrazine , hydrogen sulfide , glutathione peroxidase , chemistry , pharmacology , ischemia , intestinal ischemia , pathophysiology , antioxidant , medicine , biochemistry , pathology , sulfur , alternative medicine , organic chemistry
Objectives Hydrogen sulfide (H 2 S) is an endogenously gaseous mediator, regulating many pathophysiological functions in mammalian cells. H 2 S has been shown to inhibit myocardial ischaemia–reperfusion (I/R) injury. However, little is known about whether H 2 S could modulate intestinal I/R injury. This study aimed to investigate the effect of H 2 S on intestinal I/R injury and potential mechanism(s) underlying the action of H 2 S 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 H 2 S donor at 7 or 14 μmol/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. Key findings 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 H 2 S protects from intestinal I/R injury in rats, which is associated with increase in the activity of antioxidant enzymes.