Helicobacter pylori attenuates the delay in ulcer healing induced by aspirin and selective COX-2 inhibitor

被引：0

作者：

Brzozowski T. ^{[1
]}

Konturek P.C. ^{[2
]}

Sliwowski Z. ^{[1
]}

Konturek S. ^{[1
]}

Bielanski W. ^{[1
]}

Pajdo R. ^{[1
]}

Drozdowicz D. ^{[1
]}

Hahn E. ^{[1
]}

机构：

[1] Department of Physiology, Jagiellonian Univ. Sch. of Medicine, 31-531 Cracow

[2] Department of Medicine I, University Erlangen-Nuremberg, Erlangen

来源：

InflammoPharmacology | 2002年 / 10卷 / 4-6期

关键词：

ASA; Gastric blood flow; Gastric secretion; Gastrin; Helicobacter pylori; Rofecoxib; Ulcer healing;

D O I：

10.1163/156856002321544891

中图分类号：

学科分类号：

摘要：

Helicobacter pylori (H. pylori) and NSAIDs are recognized as major pathogenic factors in peptic ulcer disease. However, whether these two factors exert synergistic or antagonistic effects on ulcer healing has not yet been fully explained. In this study, the effects of aspirin (ASA) alone and rofecoxib, a specific prostaglandin cyclooxygenase (COX)-2 inhibitor, were compared with that of ASA and rofecoxib applied in combination with H. pylori on gastric acid secretion and healing of acetic acid ulcers in rats. The H. pylori colonization of gastric mucosa was determined by viable bacterial culture and histology. The area of ulcers was determined by planimetry, the gastric blood flow (GBF) was measured using the H2-gas clearance method and the gastric mucosal generation of PGE2 and plasma gastrin levels were assessed by radioimmunoassay. ASA or rofecoxib applied alone delayed significantly the healing of chronic gastric ulcers and this effect was accompanied by a marked decrease in the GBF at the ulcer margin and gastric mucosal PGE2 generation without significant influence of gastric acid output. H. pylori that produced moderate gastric inflammation at the ulcer margin as confirmed by bacterial culture, prolonged significantly the healing of these ulcers and decreased the GBF at the ulcer margin and gastric acid output while elevating significantly the gastric mucosal PGE2 generation and plasma gastrin levels. H. pylori attenuated significantly the ASA- and rofecoxib-induced inhibition of ulcer healing and accompanying fall in the GBF at the ulcer margin and reversed, in part, the ASA- and rofecoxib-induced alterations in PGE2 generation. We conclude that H. pylori attenuates the delay in ulcer healing induced by ASA and rofecoxib due to enhancement in the generation of endogenous PGE2 and gastrin release, as well as suppression of acid secretion which may limit deleterious influence of NSAID on ulcer healing.

引用

页码：423 / 433

页数：10

共 28 条

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