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

Authors
 Joo Weon Lim  ;  Hyeyoung Kim  ;  Kyung Hwan Kim 
Citation
 FREE RADICAL BIOLOGY AND MEDICINE, Vol.31(3) : 355-366, 2001 
Journal Title
 FREE RADICAL BIOLOGY AND MEDICINE 
ISSN
 0891-5849 
Issue Date
2001
MeSH
Antioxidants/pharmacology ; Apoptosis* ; Catalase/pharmacology ; Cell Line ; Cell Survival/drug effects ; Enzyme Induction ; Gastric Mucosa/cytology ; Gastric Mucosa/drug effects ; Gastric Mucosa/microbiology* ; Gastric Mucosa/physiology ; Gene Expression Regulation, Enzymologic* ; Helicobacter Infections/genetics ; Helicobacter Infections/pathology ; Helicobacter Infections/physiopathology* ; Helicobacter pylori* ; Humans ; Molsidomine/analogs & derivatives ; Molsidomine/pharmacology ; NF-kappa B/genetics ; NF-kappa B/metabolism* ; NG-Nitroarginine Methyl Ester/pharmacology ; Nitric Oxide Donors/pharmacology ; Nitric Oxide Synthase/biosynthesis ; Nitric Oxide Synthase/genetics* ; Nitric Oxide Synthase Type II ; Nitroso Compounds/pharmacology ; Oligodeoxyribonucleotides, Antisense/pharmacology ; Pyrrolidines/pharmacology ; Radiation-Protective Agents/pharmacology ; Thiazines/pharmacology ; Thiocarbamates/pharmacology
Keywords
Helicobacter pylori ; NF-κB ; Inducible nitric oxide synthase ; Apoptosis ; Free radicals
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.
Full Text
http://www.sciencedirect.com/science/article/pii/S0891584901005925
DOI
10.1016/S0891-5849(01)00592-5
Appears in Collections:
5. Research Institutes (연구소) > Institute of Gastroenterology (소화기병연구소) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Pharmacology (약리학교실) > 1. Journal Papers
Yonsei Authors
Kim, Kyung Hwan(김경환)
Lim, Joo Weon(임주원)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/141954
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