title: Eradication of Helicobacter pylori significantly reduced gastric damage in nonsteroidal anti-inflammatory drug-treated Mongolian gerbils.
abstract: OBJECTIVE
  To examine the effect of eradication of Helicobacter pylori prior to usage of NSAIDs, by investigating gastric inflammatory activity, myeloperoxidase (MPO) activity, prostaglandin (PG) E2 synthesis in H pylori-infected, and H pylori-eradicated gerbils followed by administration of indomethacin and rofecoxib.
  
  
  METHODS
  Six-week-old male gerbils were orally inoculated with H pylori. Seven weeks later, anti-H pylori triple therapy and vehicle were given to gerbils respectively and followed by oral indomethacin (2 mg/kg.d) or rofecoxib (10 mg/kg.d) for 2 wk. We examined the area of lesions, gastric inflammatory activity, PGE2 synthesis and MPO activity in the stomach.
  
  
  RESULTS
  In indomethacin and rofecoxib-treated gerbils, the following results were obtained in H pylori-infected group vs H pylori-eradicated group respectively: hyperplasia area of the stomach (mm2): 82.4+/-9.2 vs 13.9+/-3.5 (P<0.05), 30.5+/-5.1 vs 1.3+/-0.6 (P<0.05); erosion and ulcer area (mm2): 14.4+/-4.9 vs 0.86+/-0.5 (P<0.05), 1.3+/-0.6 vs 0.4+/-0.3 (P<0.05); score of gastritis: 7.0+/-0.0 vs 3.6+/-0.5 (P<0.05), 7.0+/-0.0 vs 2.7+/-0.5 (P<0.05); MPO activity (micromol H2O2/min/g tissue): 104.7+/-9.2 vs 9.0+/-2.3 (P<0.05), 133.5+/-15.0 vs 2.9+/-0.7 (P<0.05); PGE2 synthesis (pg/mg wet weight/min): 299.2+/-81.5 vs 102.8+/-26.2 (P<0.05), 321.4+/-30.3 vs 11.9+/-4.8 (P<0.05).
  
  
  CONCLUSIONS
  Eradication of H pylori reduced gastric damage of NSAID-treated Mongolian gerbils. Rofecoxib caused less severe gastric damage than indomethacin in H pylori-eradicated gerbils.
authors.affiliation: Division of Gastroenterology, Department of Internal Medicine, Taipei Medical University Hospital, Taipei, Taiwan, China. chunchao@tmu.edu.tw
authors.forename: Chun-Chao
authors.initials: CC
authors.lastname: Chang
authors.forename: Sheng-Hsuan
authors.initials: SH
authors.lastname: Chen
authors.forename: Gi-Shih
authors.initials: GS
authors.lastname: Lien
authors.forename: Horng-Yuan
authors.initials: HY
authors.lastname: Lou
authors.forename: Ching-Ruey
authors.initials: CR
authors.lastname: Hsieh
authors.forename: Chia-Lang
authors.initials: CL
authors.lastname: Fang
authors.forename: Shiann
authors.initials: S
authors.lastname: Pan
mesh_terms: D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D001835:Body Weight; D002908:Chronic Disease; D015232:Dinoprostone / Q000096:biosynthesis; D005756:Gastritis / Q000382:microbiology / Q000473:pathology; D005849:Gerbillinae; D016481:Helicobacter Infections / Q000188:drug therapy / Q000473:pathology*; D016480:Helicobacter pylori; D007213:Indomethacin / Q000494:pharmacology*; D007783:Lactones / Q000494:pharmacology*; D008297:Male; D009929:Organ Size; D009195:Peroxidase / Q000378:metabolism; D013270:Stomach / Q000187:drug effects / Q000382:microbiology / Q000473:pathology; D013276:Stomach Ulcer / Q000139:chemically induced / Q000473:pathology; D013450:Sulfones / Q000494:pharmacology*
chemical_list: D000900:Anti-Bacterial Agents; D000894:Anti-Inflammatory Agents, Non-Steroidal; D007783:Lactones; D013450:Sulfones; C116926:rofecoxib; D009195:Peroxidase; D015232:Dinoprostone; D007213:Indomethacin