NF-κB, inducible nitric oxide synthase and apoptosis by Helicobacter pylori infection

Joo Weon Lim, Hye Young Kim, Kyung Hwan Kim

Research output: Contribution to journalArticle

69 Citations (Scopus)

Abstract

Oxygen radicals are considered as an important regulator in the pathogenesis of Helicobacter pylori (H. pylori)-induced gastric ulceration and carcinogenesis. Inflammatory genes including inducible nitric oxide synthase (iNOS) may be regulated by oxidant-sensitive transcription factor, nuclear factor-κB (NF-κB). iNOS induction has been related to gastric apoptosis. We studied the role of NF-κB on iNOS expression and apoptosis in H. pylori-stimulated gastric epithelial AGS cells. AGS cells were treated with antisense oligonucleotide (AS ODN) for NF-κB subunit p50, an antioxidant enzyme catalase, an inhibitor of NF-κB activation pyrrolidine dithiocarbamate (PDTC), iNOS inhibitors NG-nitro-L-arginine-methyl ester (L-NAME) and 2-amino-5,6-dihydro-6-methyl-4H-1,3-thiazine (AMT), a peroxynitrite donor SIN-1, and a nitric oxide donor NOC-18 in the presence or absence of H. pylori. H. pylori induced cytotocixity time- and dose-dependently, which occurred with induction in iNOS expression and nitrite production. SIN-1 and NOC-18 induced dose-dependent cytotoxicity in AGS cells. Catalase, PDTC, L-NAME, and AMT prevented H. pylori-induced cytotoxicity and apoptosis. It was related to their inhibition on iNOS expression and nitrite production. The cells treated with AS ODN had low levels of p50 and NF-κB and inhibited H. pylori-induced cytotoxicity, apoptosis, iNOS expression, and nitrite production. In conclusion, NF-κB plays a novel role in iNOS expression and apoptosis in H. pylori-infected gastric epithelial cells.

Original languageEnglish
Pages (from-to)355-366
Number of pages12
JournalFree Radical Biology and Medicine
Volume31
Issue number3
DOIs
Publication statusPublished - 2001 Aug 1

Fingerprint

Helicobacter Infections
Nitric Oxide Synthase Type II
Helicobacter pylori
Apoptosis
NG-Nitroarginine Methyl Ester
Stomach
Cytotoxicity
Nitrites
Catalase
Epithelial Cells
Peroxynitrous Acid
Nitric Oxide Donors
Antisense Oligonucleotides
Enzyme Inhibitors
Oxidants
Reactive Oxygen Species
Carcinogenesis
Transcription Factors
Antioxidants
Genes

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Physiology (medical)

Cite this

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abstract = "Oxygen radicals are considered as an important regulator in the pathogenesis of Helicobacter pylori (H. pylori)-induced gastric ulceration and carcinogenesis. Inflammatory genes including inducible nitric oxide synthase (iNOS) may be regulated by oxidant-sensitive transcription factor, nuclear factor-κB (NF-κB). iNOS induction has been related to gastric apoptosis. We studied the role of NF-κB on iNOS expression and apoptosis in H. pylori-stimulated gastric epithelial AGS cells. AGS cells were treated with antisense oligonucleotide (AS ODN) for NF-κB subunit p50, an antioxidant enzyme catalase, an inhibitor of NF-κB activation pyrrolidine dithiocarbamate (PDTC), iNOS inhibitors NG-nitro-L-arginine-methyl ester (L-NAME) and 2-amino-5,6-dihydro-6-methyl-4H-1,3-thiazine (AMT), a peroxynitrite donor SIN-1, and a nitric oxide donor NOC-18 in the presence or absence of H. pylori. H. pylori induced cytotocixity time- and dose-dependently, which occurred with induction in iNOS expression and nitrite production. SIN-1 and NOC-18 induced dose-dependent cytotoxicity in AGS cells. Catalase, PDTC, L-NAME, and AMT prevented H. pylori-induced cytotoxicity and apoptosis. It was related to their inhibition on iNOS expression and nitrite production. The cells treated with AS ODN had low levels of p50 and NF-κB and inhibited H. pylori-induced cytotoxicity, apoptosis, iNOS expression, and nitrite production. In conclusion, NF-κB plays a novel role in iNOS expression and apoptosis in H. pylori-infected gastric epithelial cells.",
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NF-κB, inducible nitric oxide synthase and apoptosis by Helicobacter pylori infection. / Lim, Joo Weon; Kim, Hye Young; Kim, Kyung Hwan.

In: Free Radical Biology and Medicine, Vol. 31, No. 3, 01.08.2001, p. 355-366.

Research output: Contribution to journalArticle

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