In:
American Journal of Physiology-Gastrointestinal and Liver Physiology, American Physiological Society, Vol. 285, No. 6 ( 2003-12), p. G1171-G1180
Abstract:
Helicobacter pylori infection induces apoptosis and inducible nitric oxide synthase (iNOS) expression in gastric epithelial cells. In this study, we investigated the effects of NF-κB activation and iNOS expression on apoptosis in H. pylori-infected gastric epithelial cells. The suppression of NF-κB significantly increased caspase-3 activity and apoptosis in H. pylori-infected MKN-45 and Hs746T gastric epithelial cell lines as well as primary gastric epithelial cells. An NF-κB signaling pathway via NF-κB-inducing kinase and IκB kinase-β activation was found to be involved in the inhibition of apoptosis in H. pylori-infected gastric epithelial cells. In gastric epithelial cells transfected with retrovirus containing IκBα superrepressor, iNOS mRNA and protein levels were reduced, indicating that H. pylori infection induced the expression of iNOS by activating NF-κB. Moreover, a NO donor, S-nitroso- N-acetylpenicillamine (100 μM), decreased caspase-3 activity and apoptosis in NF-κB-suppressed cells infected with H. pylori. These results suggest that NF-κB activation may play a role in protecting gastric epithelial cells from H. pylori-induced apoptosis by upregulating endogenous iNOS.
Type of Medium:
Online Resource
ISSN:
0193-1857
,
1522-1547
DOI:
10.1152/ajpgi.00502.2002
Language:
English
Publisher:
American Physiological Society
Publication Date:
2003
detail.hit.zdb_id:
1477329-6
SSG:
12
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