Cookies Policy

This site uses cookies. By continuing to browse the site you are agreeing to our use of cookies.

I accept this policy

Find out more here

Oxidative stress in Helicobacter pylori-induced gastric cell injury

No metrics data to plot.
The attempt to load metrics for this article has failed.
The attempt to plot a graph for these metrics has failed.
The full text of this article is not currently available.

Brill’s MyBook program is exclusively available on BrillOnline Books and Journals. Students and scholars affiliated with an institution that has purchased a Brill E-Book on the BrillOnline platform automatically have access to the MyBook option for the title(s) acquired by the Library. Brill MyBook is a print-on-demand paperback copy which is sold at a favorably uniform low price.

Access this article

+ Tax (if applicable)
Add to Favorites
You must be logged in to use this functionality

image of Inflammopharmacology

Oxygen radicals are supposed to be involved in inflammation and cell proliferation. Helicobacter pylori induces decrease in antioxidant defense factors, such as GSH, mucus and constitutive nitric oxide (NO), gastric mucosal injury and inflammation. Inflammation and injury might be caused by oxidant-mediated expression of inflammatory cytokine interleukin-8 (IL-8) and inflammatory enzymes such as cyclooxtgenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), which were mediated by oxidant-sensitive transcription factors such as nuclear factor-κB (NF-κB) and activator protein-1 (AP-1), possibly with mitogen activated protein kinase (MAPK) activation. H. pylori-induced alterations in protein expression demonstrate the involvement of oxidative stress in the pathogenesis of H. pylori-induced gastric diseases. The differentially expressed genes and proteins may be useful as prognostic indices for gastric diseases associated with H. pylori infection. In conclusion, oxygen radicals are produced in gastric epithelial cells infected with H. pylori, which may reduce the antioxidant defense mechanism and turn on the expression of inflammatory genes, adhesion molecules and mediators stimulating cell proliferation, as well as defensive molecular chaperones in gastric epithelial cells.

Affiliations: 1: Department of Pharmacology and Institute of Gastroenterology, Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, Seoul 120-752, South Korea


Full text loading...


Data & Media loading...

Article metrics loading...



Can't access your account?
  • Tools

  • Add to Favorites
  • Printable version
  • Email this page
  • Subscribe to ToC alert
  • Get permissions
  • Recommend to your library

    You must fill out fields marked with: *

    Librarian details
    Your details
    Why are you recommending this title?
    Select reason:
    Inflammopharmacology — Recommend this title to your library
  • Export citations
  • Key

  • Full access
  • Open Access
  • Partial/No accessInformation