AIM:To investigate the effects of sodium alginate(ALNa)on indomethacin-induced small intestinal lesions in rats.METHODS:Gastric injury was assessed by measuring ulcerated legions 4 h after indomethacin(25 mg/kg)administration.Small intestinal injury was assessed by measuring ulcerated legions 24 h after indomethacin(10mg/kg)administration.AL-Na and rebamipide were orally administered.Myeloperoxidase activity in the stomach and intestine were measured.Microvascular permeability,superoxide dismutase content,glutathione peroxidase activity,catalase activity,red blood cell count,white blood cell count,mucin content and enterobacterial count in the small intestine were measured.RESULTS:AL-Na significantly reduced indomethacininduced ulcer size and myeloperoxidase activity in the stomach and small intestine.AL-Na prevented increases in microvascular permeability,superoxide dismutase content,glutathione peroxidase activity and catalase activity in small intestinal injury induced by indomethacin.AL-Na also prevented decreases in red blood cells and white blood cells in small intestinal injury induced by indomethacin.Moreover,AL-Na suppressed mucin depletion by indomethacin and inhibited infiltration of enterobacteria into the small intestine.CONCLUSION:These results indicate that AL-Na ameliorates non-steroidal anti-inflammatory drug-induced small intestinal enteritis via bacterial translocation. AIM: To investigate the effects of sodium alginate (ALNa) on indomethacin-induced small intestinal vessels in rats. METHODS: Gastric injury was assessed by measuring ulcerated leg 4 h after indomethacin (25 mg / kg) administration. measuring ulcerated legions 24 h after indomethacin (10 mg / kg) administration. AL-Na and rebamipide were orally administered. Myeloperoxidase activity in the stomach and intestine were measured. Micrvascular permeability, superoxide dismutase content, glutathione peroxidase activity, catalase activity, red blood cell count, white blood cell count, mucin content and enterobacterial count in the small intestine were measured .RESULTS: AL-Na significantly reduced indomethacininduced ulcer size and myeloperoxidase activity in the stomach and small intestine. AL-Na increases increases in microvascular permeability, superoxide dismutase content, glutathione peroxidase activity and catalase activity in small intestinal injury induced by indomethac in. AL-Na also prevents decreased in red blood cells and white blood cells in small intestinal injury induced by indomethacin. Moreover, AL-Na suppressed mucin depletion by indomethacin and inhibited infiltration of enterobacteria into the small intestine. CONCLUSION: These results indicate that AL-Na ameliorates non-steroidal anti-inflammatory drug-induced small intestinal enteritis via bacterial translocation.