AIM:To investigate the protective effect of lansoprazoleon ischemia and reperfusion(I/R)-induced rat intestinalmucosal injury in vivo.METHODS:Intestinal damage was induced by clampingboth the superior mesenteric artery and the celiac trunkfor 30 rain followed by reperfusion in male Sprague-Dawleyrats.Lansoprazole was given to rats intraperitoneally 1 hbefore vascular clamping.RESULTS:Both the intraluminal hemoglobin and proteinlevels,as indices of mucosal damage,significantlyincreased in I/R-groups comparion with those of sham-operation groups.These increases in intraluminal hemoglobinand protein levels were significantly inhibited by the treatmentwith lansoprazole at a dose of 1 mg/kg.Small intestineexposed to I/R resulted in mucosal inflammation that wascharacterized by significant increases in thiobarbituric acid-reactive substances(TBARS),tissue-associatedmyeloperoxidase activity(MPO),and mucosal content of ratcytokine-induced neutrophil chemoattractant-1(CINC-1).These increases in TBARS,MPO activities and CINC-1 contentin the intestinal mucosa after I/R were all inhibited bypretreatment with lansoprazole at a dose of 1 mg/kg.Furthermore,the CINC-1 mRNA expression was increasedduring intestinal I/R,and this increase in mRNA expressionwas inhibited by treatment with lansoprazole.CONCLUSION:Lansoprazole inhibits lipid peroxidation andreduces development of intestinal mucosal inflammationinduced by I/R in rats,suggesting that lansoprazole mayhave a therapeutic potential for I/R injury. AIM: To investigate the protective effect of lansoprazoleon ischemia and reperfusion (I / R) -induced rat intestinal mucosal injury in vivo. METHODS: Intestinal damage was induced by clampingboth the superior mesenteric artery and the celiac trunk for 30 min followed by reperfusion in male Sprague- Dawleyrats. Lansoprazole was given to rats intraperitoneally 1 hbefore vascular clamping .RESULTS: Both the intraluminal hemoglobin and proteinlevels, as indices of mucosal damage, significantly increased in I / R-groups comparion with those of sham-operation groups. These increases in intraluminal hemoglobin and protein levels were significantly inhibited by the treatment with lansoprazole at a dose of 1 mg / kg. Small intestineexposed to I / R resulted in mucosal inflammation that was characterized by significant increases in thiobarbituric acid-reactive substances (TBARS), tissue-associated myeloperoxidase activity (MPO), and mucosal content of ratcytokine-induced neutrophil chemoattractant-1 (CINC-1) .These increases in TBARS, MPO activities and CINC-1 contentin the intestinal mucosa after I / R were all inhibited by treatment with lansoprazole at a dose of 1 mg / kg. Fermentmore, the CINC-1 mRNA expression was increased to intestinal I / R, and this increase in mRNA expressionwas inhibited by treatment with lansoprazole. CONCLUSION: Lansoprazole inhibits lipid peroxidation andreduces development of intestinal mucosal inflammation induced by I / R in rats, suggesting that lansoprazole mayhave a therapeutic potential for I / R injury.