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Effects of nonsteroidal anti-inflammatory drugs on Helicobacter pylori-infected gastric mucosae of mice: apoptosis, cell proliferation, and inflammatory activity.

Authors
Kim, TI; Lee, YC; Lee, KH; Han, JH; Chon, CY; Moon, YM; Kang, JK; Park, IS
Citation
Infection and immunity, 69(8):5056-5063, 2001
Journal Title
Infection and immunity
ISSN
0019-95671098-5522
Abstract
Helicobacter pylori and nonsteroidal anti-inflammatory drugs (NSAIDs) are two well-known important causative factors of gastric damage. While H. pylori increases apoptosis and the proliferation of gastric epithelial cells and is an important factor in peptic ulcer and gastric cancer, NSAIDs induce cell apoptosis and have antineoplastic effects. We investigated the effects of NSAIDs (a nonselective cyclooxygenase [COX] inhibitor [indomethacin] and a selective COX-2 inhibitor [NS-398]) on the apoptosis and proliferation of gastric epithelial cells and gastric inflammation in H. pylori-infected mice. C57BL/6 mice were sacrificed 8 weeks after H. pylori SS1 inoculation. Indomethacin (2 mg/kg) or NS-398 (10 mg/kg) was administered subcutaneously once daily for 10 days before sacrifice. The following were assessed: gastric inflammatory activity, gastric COX protein expression by Western blotting; gastric prostaglandin E(2) levels by enzyme immunoassay, apoptosis by terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling, and cell proliferation by Ki67 immunostaining. Compared to the controls, H. pylori infection and/or NSAID treatment increased COX-1 and COX-2 protein expression. Gastric prostaglandin E(2) levels, apoptotic index, cell proliferation index, neutrophil activity, and the degree of chronic inflammation were all increased by H. pylori infection, and these effects were significantly decreased by indomethacin treatment. However, NS-398 treatment after H. pylori infection did not induce a significant reduction, although it did result in a tendency to decrease. These results show that NSAIDs can reverse the increased apoptosis and proliferation of epithelial cells and inflammatory activity in the stomachs of H. pylori-infected mice and that, like COX-2 activation, COX-1 induction contributes to the change of gastric mucosal cell turnover and inflammation induced by H. pylori infection.
MeSH terms
AnimalsAnti-Inflammatory Agents, Non-Steroidal/pharmacology*Apoptosis/drug effects*Apoptosis/immunologyCell DivisionChronic DiseaseCyclooxygenase 1Cyclooxygenase 2Cyclooxygenase 2 InhibitorsCyclooxygenase Inhibitors/pharmacologyDinoprostone/metabolismDisease Models, AnimalEpithelial Cells/cytologyFemaleGastric Mucosa/cytologyGastric Mucosa/drug effects*Gastric Mucosa/immunologyGastritis/immunology*Gastritis/pathologyHelicobacter Infections/immunology*Helicobacter Infections/pathologyHelicobacter pylori/immunology*HumansIndomethacin/pharmacology*Isoenzymes/antagonists & inhibitorsIsoenzymes/biosynthesisMembrane ProteinsMiceMice, Inbred C57BLNitrobenzenes/pharmacology*Prostaglandin-Endoperoxide Synthases/biosynthesisSulfonamides/pharmacology*
DOI
10.1128/IAI.69.8.5056-5063.2001
PMID
11447186
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Pathology
AJOU Authors
한, 재호
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