Objectives Hydrogen sulfide (H,S) 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 H,S 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, all H2S donor at 7 or 14 mu mol/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 (NIDA), 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.