Effect of mannitol on Helicobacter pylori-induced cyclooxygenase-2 expression in gastric epithelial AGS cells

Hyeyoung Kim, Jeong Yeon Seo, Kyung Hwan Kim

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Oxygen radicals have been considered to be important regulatory molecules in Helicobacter pylori-induced gastric ulceration and carcinogenesis. H. pylori-induced inflammation has been shown to be associated with cyclooxygenase-2 (COX-2) expression in experimental animals and human patients. This study aimed to determine if H. pylori produces oxygen radicals and induces COX-2 expression in gastric epithelial cells. A further aim was to resolve whether or not the H. pylori-induced COX-2 expression could be inhibited by mannitol, a known hydroxyl radical scavenger, and superoxide dismutase (SOD), an antioxidant enzyme, which was used as a positive control. A human gastric epithelial cell line, AGS, treated with or without mannitol or SOD, was incubated in the presence or absence of H. pylori. mRNA expression and protein levels for COX-2 were determined by Northern blot and Western blot analysis, respectively. Levels of the COX-2 products, 6-keto-prostaglandin F (6-keto-PGF) and thromboxane B2 (TXB2) and H2O2 were measured in the medium. The results showed that H. pylori induced H2O2 production, COX-2 mRNA and protein expression and increased the levels of 6-keto-PGF and TXB2. The H. pylori-induced COX-2 expression and the increase in the COX-2 products were inhibited by both mannitol and SOD. The inhibitory effect of mannitol on H. pylori-induced COX-2 expression suggests the possible involvement of oxygen radicals in the transcriptional regulation of the inflammatory mediators in gastric epithelial cells. Copyright

Original languageEnglish
Pages (from-to)182-189
Number of pages8
JournalPharmacology
Volume66
Issue number4
DOIs
Publication statusPublished - 2002 Dec 1

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Mannitol
Cyclooxygenase 2
Helicobacter pylori
Stomach
Epithelial Cells
Superoxide Dismutase
Reactive Oxygen Species
Thromboxane B2
Messenger RNA
Northern Blotting
Hydroxyl Radical
Carcinogenesis
Proteins
Antioxidants
Western Blotting
Inflammation
Cell Line
Enzymes

All Science Journal Classification (ASJC) codes

  • Pharmacology

Cite this

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abstract = "Oxygen radicals have been considered to be important regulatory molecules in Helicobacter pylori-induced gastric ulceration and carcinogenesis. H. pylori-induced inflammation has been shown to be associated with cyclooxygenase-2 (COX-2) expression in experimental animals and human patients. This study aimed to determine if H. pylori produces oxygen radicals and induces COX-2 expression in gastric epithelial cells. A further aim was to resolve whether or not the H. pylori-induced COX-2 expression could be inhibited by mannitol, a known hydroxyl radical scavenger, and superoxide dismutase (SOD), an antioxidant enzyme, which was used as a positive control. A human gastric epithelial cell line, AGS, treated with or without mannitol or SOD, was incubated in the presence or absence of H. pylori. mRNA expression and protein levels for COX-2 were determined by Northern blot and Western blot analysis, respectively. Levels of the COX-2 products, 6-keto-prostaglandin F1α (6-keto-PGF1α) and thromboxane B2 (TXB2) and H2O2 were measured in the medium. The results showed that H. pylori induced H2O2 production, COX-2 mRNA and protein expression and increased the levels of 6-keto-PGF1α and TXB2. The H. pylori-induced COX-2 expression and the increase in the COX-2 products were inhibited by both mannitol and SOD. The inhibitory effect of mannitol on H. pylori-induced COX-2 expression suggests the possible involvement of oxygen radicals in the transcriptional regulation of the inflammatory mediators in gastric epithelial cells. Copyright",
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Effect of mannitol on Helicobacter pylori-induced cyclooxygenase-2 expression in gastric epithelial AGS cells. / Kim, Hyeyoung; Seo, Jeong Yeon; Kim, Kyung Hwan.

In: Pharmacology, Vol. 66, No. 4, 01.12.2002, p. 182-189.

Research output: Contribution to journalArticle

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