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

Involvement of interleukin-4 in down-regulation of endothelin-1 during gastric ulcer healing: Effect of ebrotidine

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

Aims: Healing gastric mucosal injury implies an orderly involvement of the signaling molecules that exert their influence on the processes leading to the restoration of the mucosal integrity. In this study, we investigated the effect of antiulcer agent, ebrotidine, on the course of events during gastric ulcer healing by analyzing the expression of interleukin-4 (IL-4), endothelin-1 (ET-1), tumor necrosis factor-a (TNF-a), and the mucosal activity of caspase-3, and constitutive (cNOS) and inducible (NOS-2) nitric oxide synthase.Methods: Rats with experimentally induced chronic gastric ulcers were administered twice daily for 14 days with either ebrotidine at 100 mg/kg or vehicle, and at different stages of treatment their stomachs were used for macroscopic and biochemical assessments.Results: The ulcer onset was characterized by a massive epithelial apoptosis associated with a significant increase in caspase-3, NOS-2, TNF-a and ET-1, and a decline in the mucosal expression of cNOS and IL-4. The healing was reflected in a rapid recovery in IL-4, decrease in apoptosis, caspase-3, TNF-a, ET-1 and NOS-2, and a slow recovery in cNOS, and the process was accelerated in the ebrotidine-treated group. In the absence of ebrotidine the expression of IL-4 returned to the level of normal mucosa by the seventh day of healing, and that of ET-1 and TNF-a by the fourteenth day. An accelerated ulcer healing (7 days) with ebrotidine treatment was associated with IL-4 recovery by the fourth day, ET-1 by the seventh day, and TNF-a and cNOS by the 10th day. However, in both groups of animals the apoptotic DNA fragmentation rate, and the expression of caspase-3 and NOS-2 remained significantly elevated even after the ulcer healed.Conclusions: Our findings suggest that a drop in the mucosal expression of IL-4 at the ulcer onset causes dysregulation of ET-1 production, induction of TNF-a and triggers the apoptotic events that affect the efficiency of the repair process. Ebrotidine, by eliciting rapid recovery in IL-4, is capable of suppression the mucosal apoptotic events and accelerate the ulcer healing.


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