BACKGROUND/AIMS: The prevalence of peptic ulcer disease has not decreased mainly due to an increase in the use of NSAIDs. This study was conducted in order to determine whether a chronic NSAID-induced gastric inflammation model could be established by repeated administration of NSAID. METHODS: Indomethacin (10 mg/kg) was administered once per week for six weeks in 8- and 26-week rats and animals were sacrificed every week after administration. Gross ulcer index, histologic damage index, myeloperoxidase (MPO) activity, and mucus (glucosamine) levels were measured. Small bowel damage was also evaluated. RESULTS: Gross gastric damage index showed a peak level at three weeks and then decreased slowly in the 26-week indomethacin group. Gastric mucosal glucosamine level increased in both the 8-week (p=0.038) and 26-week groups (p=0.007). In addition, gastric mucosal MPO level decreased in the 8-week group (p=0.018) but did not show a decrease in the 26-week group. Small bowel damage began to occur at three weeks during the schedule and eight of 36 rats (22.2%) died due to perforation or peritonitis of the small bowel in the 8- and 26-week indomethacin groups, respectively. CONCLUSIONS: Due to gastric adaptation and small bowel damage, repeated administration of NSAID to experimental animals may not be an adequate method for establishment of the chronic gastric inflammation model.
Animals ; Anti-Inflammatory Agents, Non-Steroidal/*toxicity ; Disease Models, Animal ; Gastric Mucosa/*drug effects/enzymology/pathology ; Glucosamine/metabolism ; Indomethacin/*toxicity ; Intestine, Small/*drug effects/pathology ; Male ; Peroxidase/metabolism ; Rats ; Rats, Sprague-Dawley ; Time Factors

BACKGROUND/AIMS: The prevalence of peptic ulcer disease has not decreased mainly due to an increase in the use of NSAIDs. This study was conducted in order to determine whether a chronic NSAID-induced gastric inflammation model could be established by repeated administration of NSAID. METHODS: Indomethacin (10 mg/kg) was administered once per week for six weeks in 8- and 26-week rats and animals were sacrificed every week after administration. Gross ulcer index, histologic damage index, myeloperoxidase (MPO) activity, and mucus (glucosamine) levels were measured. Small bowel damage was also evaluated. RESULTS: Gross gastric damage index showed a peak level at three weeks and then decreased slowly in the 26-week indomethacin group. Gastric mucosal glucosamine level increased in both the 8-week (p=0.038) and 26-week groups (p=0.007). In addition, gastric mucosal MPO level decreased in the 8-week group (p=0.018) but did not show a decrease in the 26-week group. Small bowel damage began to occur at three weeks during the schedule and eight of 36 rats (22.2%) died due to perforation or peritonitis of the small bowel in the 8- and 26-week indomethacin groups, respectively. CONCLUSIONS: Due to gastric adaptation and small bowel damage, repeated administration of NSAID to experimental animals may not be an adequate method for establishment of the chronic gastric inflammation model.
Animals ; Anti-Inflammatory Agents, Non-Steroidal/*toxicity ; Disease Models, Animal ; Gastric Mucosa/*drug effects/enzymology/pathology ; Glucosamine/metabolism ; Indomethacin/*toxicity ; Intestine, Small/*drug effects/pathology ; Male ; Peroxidase/metabolism ; Rats ; Rats, Sprague-Dawley ; Time Factors

OBJECTIVETo study the effects and its possible mechanisms of total alkaloids (TA) from rhizoma Coptis chinensis on H. pylori LPS induced gastric lesion in rats.

METHODH. pylori lipopolysaccharide was applied to rat intragastrically for 4 days to induce a pattern of mucosal responses resembling that of acute gastritis. After treatment with 50, 100, 200 mg x kg(-1) TA, we identified the changes on gastric histopathology, the effects on the activities of cNOS and NOS-2, the contents of TNF-alpha and the gastric mucus epithelial cell apoptosis.

RESULTH. pylori LPS could significantly induce the epithelial cell apoptosis of gastric mucus, increase the expression of NOS-2 and decline the expression of cNOS, and enhance the content of TNF-alpha in serum. Treatment with 50, 100, 200 mg x kg(-1) TA led to reduction in the extent of mucosal inflammatory changes elicited by H. pylori LPS and decrease in epithelial cell apoptosis. Furthermore, this effect of TA was associated with decrease in content of TNF-alpha in serum, decline in NOS-2, and increase in cNOS.

CONCLUSIONThe findings suggest that TA is a potent protective agent against H. pylori LPS induced gastric mucosal inflammation. The concerned mechanisms may be related to its inhibition on epithelial cell apoptosis, and the suppression of the inflammatory responses by upregulating cNOS and interfering with the events propagated by NOS-2, and reducing the content of TNF-alpha.

Acute Disease ; Alkaloids ; isolation & purification ; pharmacology ; Animals ; Apoptosis ; drug effects ; Coptis ; chemistry ; Epithelial Cells ; drug effects ; enzymology ; pathology ; Gastric Mucosa ; drug effects ; enzymology ; pathology ; Gastritis ; blood ; chemically induced ; prevention & control ; Lipopolysaccharides ; Male ; Nitric Oxide Synthase Type II ; metabolism ; Nitric Oxide Synthase Type III ; metabolism ; Plants, Medicinal ; chemistry ; Protective Agents ; isolation & purification ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Rhizome ; chemistry ; Tumor Necrosis Factor-alpha ; blood

OBJECTIVETo investigate the therapeutic effect of cisapride on gastric injury following hemorrhagic shock resuscitation.

METHODS108 Wistar rats weighing (200 g+/-30 g) were randomly divided into a sham shock (SS) group (n=36), a hemorrhagic shock resuscitation (HS) group (n=36) and a hemorrhagic shock cisapride treated (HSC) group (n=36). Sampling at 1, 2 and 4 hours after resuscitation was done and 6 samples for each observation item were taken. The gastric blood flow volume was measured by isotope label biological microglobulin. Gastric pHi, gastric emptying, MDA and Na+-K+-ATPase of gastric mucosa were measured.

RESULTSIn the HSC group, the relative residual rate of gastric pigment decreased significantly, the gastric blood flow volume elevated; gastric pHi increased significantly at 2 hours; the level of mucosal MDA decreased at 4 hours, the activity of Na+-K+-ATPase increased and the lactic acid level in the portal vein decreased significantly compared to the HS group.

CONCLUSIONSAfter hemorrhagic shock resuscitation, cisapride contained the following functions, 1) promoting gastric emptying, 2) increasing the blood flow of gastric blood flow volume and gastric pHi, 3) depressing the lactic acid concentration of the portal vein and improving MDA volume and Na+-K+-ATPase activity of gastric mucosa. It suggests that after complementing effective circulating blood volume for hemorrhagic shock resuscitation, early use of cisapride for gastric motility is helpful for an improvement of lasting ischemia and hypoxia in stomach.

Animals ; Cisapride ; therapeutic use ; Disease Models, Animal ; Gastric Emptying ; drug effects ; Gastric Mucosa ; chemistry ; enzymology ; Gastrointestinal Agents ; therapeutic use ; Hydrogen-Ion Concentration ; drug effects ; Rats ; Rats, Wistar ; Regional Blood Flow ; drug effects ; Resuscitation ; Shock, Hemorrhagic ; complications ; therapy ; Sodium-Potassium-Exchanging ATPase ; metabolism ; Stomach ; blood supply ; pathology ; Stomach Diseases ; drug therapy ; etiology