Abstract: AIM: To investigate the effects of genistein on intestinal ischemia-reperfusion injury in rats and the possible mechanism.METHODS: Twenty-four Wistar rats were randomly divided into three groups (n = 8):sham operation group, intestinal ischemia-reperfusion injury group(model group) and genistein group.In model group, intestinal damage was induced in rats by clamping the superior mesenteric artery for 1 h, followed by 2 h of reperfusion.Genistein group received genistein 1.0 mg·kg ^-1 i.v.5 min before intestinal ischemia.In genistein group the superior mesenteric artery was o exposured without other treatment.At 2 h of reperfusion, blood samples were collected to measure plasma level of D-lactate and intestines were removed to assay histopathological changes, wet-to-dry weight (W/D) ratio, myeloperoxidase (MPO) activity and intercellular adhesion molecule-1 (ICAM-1) protein expression.RESULTS: W/D ratio, MPO activity, expression of ICAM-1 protein in the intestine tissues and D-lactate level in plasmawere significantly higher in model and genistein group than those in sham operation group (P <0.05 or 0.01).All these indices were significantly lower in genistein group than those in model group (P <0.05 or 0.01).The morphology of lung tissues in sham operation group was basically normal, that in model group was markedly damaged, and that in genistein group was lightly damaged. CONCLUSION: Genistein has protective effect on intestinal ischemia-reperfusion injury in rats.The underlying mechanism may involve an inhibition of neutrophilic recruitment and activity in intestine caused by a down-regulation of ICAM-1 expression.

Key words: genistein, ischemia-reperfusion injury, small intestine