Effects of selective cyclooxygenase-2 inhibitor and non-selective NSAIDs on Helicobacter pylori-induced gastritis in Mongolian gerbils.
BACKGROUND
It is still a point of controversy whether Helicobacter pylori-infected patients are more likely to develop mucosal damage while taking NSAIDs. Selective cyclooxygenase (COX-2) inhibitors may be associated with less severe gastric mucosal damage than conventional NSAIDs, but this association is undefined in H. pylori-induced gastritis. The aim of this study was to evaluate the effects of selective COX-2 and nonselective NSAIDs on H. pylori-induced gastritis.


METHODS
After intragastric administration of indomethacin, NS-398 or vehicle alone, once daily for 5 days in H. pylori-infected and uninfected Mongolian gerbils, we evaluated gastric mucosal damage, inflammatory cell infiltration and prostaglandin E2 (PGE2) concentration. We investigated whether H. pylori infection induced the COX-2 expression.


RESULTS
In H. pylori-uninfected groups, the indomethacin-treated group showed the highest mucosal damage score and the lowest PGE2 concentration. There was no difference in mucosal damage scores and PGE2 concentration between NS-398 and vehicle-alone treated group. In H. pylori-infected groups, there was no difference in mucosal damage scores, irrespective of the type of drugs administered. The indomethacin-treated group showed the lowest PGE2 concentration, similar to that of the NS-398 and vehicle-alone treated groups, both without H. pylori infection. Gastric neutrophil and monocyte infiltration scores were higher in H. pylori-infected groups than in uninfected groups. However, there was no difference in these scores according to the type of drugs administered, within H. pylori-infected or uninfected groups. COX-2 protein expression was observed in H. pylori-infected Mongolian gerbils but not in uninfected ones.


CONCLUSIONS
Our animal study showed that H. pylori infection induced COX-2 expression and increased prostaglandin concentration. Administration of NSAIDs decreased the prostaglandin concentration, but did not increase mucosal damage in H. pylori-induced gastritis. Selective COX-2 inhibitors, instead of conventional NSAIDs, had no beneficial effect on preventing mucosal damage in H. pylori-induced gastritis.
Bhang
Choon Sang
CS
Division of Gastroenterology, Department of Internal Medicine, The Catholic University of Korea, Seoul, Korea.
Lee
Hak Sung
HS
Kim
Sung Soo
SS
Song
Ho Jin
HJ
Sung
Yong Jick
YJ
Kim
Jin Il
JI
Chung
In Sik
IS
Sun
Hee Sik
HS
Park
Doo Ho
DH
Lee
Youn Soo
YS
D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology / Q000627:therapeutic use*; D051546:Cyclooxygenase 2; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D015232:Dinoprostone / Q000378:metabolism*; D005753:Gastric Mucosa / Q000187:drug effects / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D005756:Gastritis / Q000188:drug therapy* / Q000382:microbiology; D005849:Gerbillinae; D016481:Helicobacter Infections / Q000188:drug therapy; D016480:Helicobacter pylori; D007213:Indomethacin / Q000627:therapeutic use*; D007527:Isoenzymes / Q000037:antagonists & inhibitors / Q000378:metabolism; D008297:Male; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism
D000894:Anti-Inflammatory Agents, Non-Steroidal; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors; D007527:Isoenzymes; D051546:Cyclooxygenase 2; D011451:Prostaglandin-Endoperoxide Synthases; D015232:Dinoprostone; D007213:Indomethacin