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Updated: Jul 19, 2026

Mouse- and Human-derived Primary Gastric Epithelial Monolayer Culture for the Study of Regeneration
Published on: May 7, 2018
Influence of COX-2 and local cytokine expressions in gastric ulcer mucosa by H. pylori and NSAID
Chun-Ying Wu1, Ming-Shing Wu, Yi-Ju Chen
1Graduate Institute of Clinical Medicine, College of Medicine, National Taiwan University, Taipei.
Background/Aims:
H. pylori and NSAIDs are the two most important pathogenic factors in gastric ulcer. NSAIDs and H. pylori share common pathogenic characteristics, but have different effects in modulating COX-2 and local cytokines in gastric ulcer mucosa. This study was designed to explore the influence of COX-2 and local cytokine expressions in gastric ulcer mucosa induced by H. pylori infection and NSAID use.
Methodology:
Twenty-three patients were recruited. Sixteen subjects were infected with H. pylori. Fifteen patients used NSAIDs. Gastric biopsy specimens were obtained by endoscopy. COX-2 and local cytokine mRNA expressions were assessed by real-time RT-PCR.
Results:
COX-2 and local cytokines were over-expressed in gastric ulcer and were positively intercorrelated. H. pylori did not alter COX-2 and local cytokine expressions in gastric ulcer, but induced IL-8 and COX-2 in antral mucosa. NSAIDs inhibited COX-2 expression in gastric ulcer, but had no effect on other local cytokines. COX-2 inhibition by NSAIDs in gastric ulcer was compatible with the findings that NSAIDs delayed gastric ulcer healing.
Conclusions:
H. pylori increased IL-8 and COX-2 in the antral mucosa, but did not influence COX-2 and local cytokines in gastric ulcer. NSAIDs inhibited COX-2 in gastric ulcer and delayed gastric ulcer healing.
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