Cookies Policy
X

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

Role of peroxisome proliferator-activated receptor γ activation in gastric mucosal ulcer healing

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

Peroxisome proliferator-activated receptor-γ (PPARγ) is a ligand-dependent transcription factor, belonging to the steroid hormone receptor family, known to play a pivotal role in the resolution of inflammation. In this study, we investigated the effect of a specific PPARγ ligand, ciglitazone, on the course of gastric ulcer healing by analyzing apoptotic processes and the mucosal activity of inducible nitric oxide synthase (NOS-2), and the expression cyclooxygenases (COX-1 and COX-2) responsible for prostaglandin (PG) generation. Groups of rats with experimentally induced gastric mucosal ulcers were administered twice daily for up to14 days with ciglitazone at 5, 10, and 15 mg/kg or the vehicle, and their mucosal tissue subjected to assessment of ulcer healing rate and biochemical measurements. The ulcer onset, characterized by a massive epithelial apoptosis and up-regulation of NOS-2 and COX-2 protein expression, was reflected in a marked increase in the mucosal PGE2 generation and NOS-2 activity, whereas healing was accompanied by a decrease in apoptosis, drop in PGE2 and NOS-2 activity, and a decrease in COX-2 and NOS-2 protein expression. The mucosal expression of COX-1 protein, however, remained unchanged. Administration of ciglitazone led to a significant dose-dependent acceleration in the mucosal reduction of PGE2 generation, epithelial cell apoptosis and NOS-2 activity, and produced a marked decline in COX-2 and NOS-2 protein expression, but the rate of ulcer healing remained unaffected. Our findings with PPARγ activator, ciglitazone, thus provide evidence that the products of induced expression of NOS-2 and COX-2 enzymes, associated with the ulcer onset, do not play a significant role in gastric ulcer healing, but rather reflect a general pattern of mucosal inflammatory responses to injury.

10.1163/156856001320290615
/content/journals/10.1163/156856001320290615
dcterms_title,pub_keyword,dcterms_description,pub_author
6
3
Loading
Loading

Full text loading...

/content/journals/10.1163/156856001320290615
Loading

Data & Media loading...

http://brill.metastore.ingenta.com/content/journals/10.1163/156856001320290615
Loading

Article metrics loading...

/content/journals/10.1163/156856001320290615
2001-08-01
2016-12-10

Sign-in

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