Eradication of Helicobacter pylori significantly reduced gastric damage in nonsteroidal anti-inflammatory drug-treated Mongolian gerbils.
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.
Chang
Chun-Chao
CC
Division of Gastroenterology, Department of Internal Medicine, Taipei Medical University Hospital, Taipei, Taiwan, China. chunchao@tmu.edu.tw
Chen
Sheng-Hsuan
SH
Lien
Gi-Shih
GS
Lou
Horng-Yuan
HY
Hsieh
Ching-Ruey
CR
Fang
Chia-Lang
CL
Pan
Shiann
S
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*
D000900:Anti-Bacterial Agents; D000894:Anti-Inflammatory Agents, Non-Steroidal; D007783:Lactones; D013450:Sulfones; C116926:rofecoxib; D009195:Peroxidase; D015232:Dinoprostone; D007213:Indomethacin