Hydrogen sulfide protects from intestinal ischaemia–reperfusion injury in rats

Objectives 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 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 H₂S protects from intestinal I/R injury in rats, which is associated with increase in the activity of antioxidant enzymes.