Abstract
Egr‐1 is a key gene & transcription factor in experimental duodenal ulceration (Khomenko T et al. 2006). Role of Egr‐1 in gastric ulcer (GU) pathogenesis is unclear. We tested the hypotheses that Egr‐1 might play a role in the molecular mechanisms of experimental GU. GU was induced in male rats (150–190 g) by: immobilization (IMO) stress for 6, 12 & 24 hr; IMO stress combined with water‐immersion (IMO‐WI) for 20 min, 1 & 3 hr; ethanol (1 ml 96%, per os) for 20 min & 1 hr; aspirin (10 mg/100g, per os) for 20 min, 1 & 3 hr. Rats were euthanized immediately after ulcerogenic compound exposure. IMO‐WI stress induced rapid early up‐regulation of Egr‐1 by 1.6‐ & 1.5‐folds (p<0.05) at 20 min & 1 h and down‐regulation ‐ at 3 hr. IMO stress increased Egr‐1 levels at 6 hr (2.1‐folds, p<0.05) with gradual down‐regulation by 24 hr. Ethanol & aspirin didn't change Egr‐1 levels. IMO‐WI stress but no aspirin & ethanol increased phosphorylation of Erk1/2 by 2.2; 2.6; 2.5‐folds at 20 min, 1 & 3 hr (p<0.01), respectively & didn't change ‐ p38. Erk2 was the major isoform expressed & phosphorylated.ConclusionEgr‐1 plays a role in the early stages of stress‐induced GU development vs. aspirin or ethanol; Erk1/2 might regulate Egr‐1 activity during stress‐induced GU.
Published Version
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