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

Blockade of p38 mitogen-activated protein kinase pathway inhibits inducible nitric oxide synthase and gastric mucosal inflammatory reaction to Helicobacter pylori lipopolysaccharide

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

Infection with Helicobacter pylori is recognized as a primary factor in the etiology of gastric disease and its early pathogenic effects are manifested by up-regulation in proinflammatory cytokine release, enhancement in nitric oxide generation, and amplification of apoptotic events. We applied the animal model of H. pylori -induced gastritis to study the effect of a specific inhibitor of p38 mitogen-activated protein kinase (p38 MAPK), SB 203580, on the mucosal apoptotic processes, and the expression of inducible nitric oxide synthase (NOS-2) activity and soluble tumor necrosis factor-α (TNF-α). Groups of rats were pretreated intragastrically with SB 203580 (5, 10, and 20 mg/kg) or vehicle, followed 60 min later by intragastric application of H. pylori lipopolysaccharide at 50 μg/animal, and after 2 and 4 additional days on the twice daily regimen of SB 203580 or vehicle, the animals were killed and their gastric mucosal tissue subjected to histologic and biochemical assessment. In the absence of SB 203580, H. pylori lipopolysaccharide elicited within 2 days a pattern of acute mucosal inflammatory responses resembling that of acute gastritis which reached a maximum by the 4th day and were accompanied by an 11.6-fold enhancement in epithelial cell apoptosis, an 8.8-fold increase in the expression of soluble TNF-α, and a 6.5-fold induction in NOS-2 activity. Administration of SB 203580 produced dose-dependent reduction (up to 58.7%) in the severity of mucosal inflammatory involvement elicited by H. pylori lipopolysaccharide and this effect of the agent was reflected in a marked reduction (up to 72.9%) in the lipopolysaccharide-induced NOS-2 expression, decline (up to 57.4%) in epithelial cell apoptosis, and a decrease (up to 51.5%) in the mucosal level of soluble TNF-α. Our findings thus suggest that the p38 MAPK signaling pathway plays a key role in H. pylori lipopolysaccharide-induced gastric mucosal inflammatory responses leading to up-regulation of apoptotic events and induction of NOS-2 expression.


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