Relationship between ethanol-induced gastritis and gastric ulcer formation in rats.
OBJECTIVE
Patients with peptic ulcer diseases have a high prevalence of coexisting chronic gastritis. The mechanism of how gastritis leads to gastric ulcer formation is yet to be determined. The purpose of this study was to clarify the relationship between gastritis and gastric ulcer in rats.


METHODS
Ethanol (80% v/v, p.o.) was given repeatedly in rats to induce subchronic gastritis. Gastric ulcer was then induced by 60% acetic acid.


RESULTS
Findings showed that subchronic gastritis potentiated gastric ulcer formation. It also produced more apoptotic cells, together with an overexpression of tumor necrosis factor-alpha (TNF alpha) in the gastric mucosa. Inhibition of the production/release of TNF alpha by pentoxifylline prevented the increase in apoptosis and the enhancement of susceptibility to ulcerative damage by subchronic gastritis. However, such subchronic gastritis did not further affect the rate of ulcer healing in these animals.


CONCLUSIONS
The induction of gastritis resulted in an activation of TNF alpha expression followed by apoptosis in the gastric mucosa. This could lead to an increase in the severity of ulcerative damage in the stomach.
Liu
E S
ES
Department of Pharmacology, Faculty of Medicine, University of Hong Kong, China.
Cho
C H
CH
D000818:Animals; D017209:Apoptosis; D002492:Central Nervous System Depressants / Q000008:administration & dosage / Q000009:adverse effects*; D004195:Disease Models, Animal; D000431:Ethanol / Q000008:administration & dosage / Q000009:adverse effects*; D005753:Gastric Mucosa / Q000378:metabolism / Q000473:pathology; D005756:Gastritis / Q000139:chemically induced* / Q000150:complications; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D013276:Stomach Ulcer / Q000209:etiology*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
D002492:Central Nervous System Depressants; D014409:Tumor Necrosis Factor-alpha; D000431:Ethanol