Aspirin Can Elicit The Recurrence of Gastric Ulcer Induced with Acetic Acid in Rats

Abstract

This study was supported by grants of New Ideas Capability for Backbone Teachers in Universities of Heilongjiang and of Scientific Research foundation in Qiqihar Medical College. Background/ Aims: Ulcer recurrence and poor healing may be critically important to the development of serious gastrointestinal complications in patients with long-term non-steroid anti-inflammatory drugs (NSAIDs). The present study is to investigate the effects of aspirin on ulcer recurrence and healing quality and to explore the mechanism. Methods: Gastric ulcers were induced with acetic acid in rats; aspirin was administrated by gavage from day 25 to day 54 after ulcer induction. The gastric juice volume, pH, gastric mucus, gastric mucosal blood flow (GMBF) and prostaglandin E₂ (PGE₂) were measured. The mRNA transcription of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) were analyzed with RT-PCR and protein expression with Western blot. Results: The gastric juice volume was significantly increased in aspirin group compared with those of fasting or saline control groups (P<0.01); while the pH, mucus, GMBF and PGE₂ were significantly decreased in aspirin treated rats compared with those of other two groups (P<0.01). COX-2, evaluated with mRNA and protein expression, was significantly augmented in aspirin group compared with others. The quality of ulcer healing (QOUH) in Aspirin group was poorer than that of fasting or saline control groups. Conclusions: Aspirin enhance the recurrence of gastric ulcer. The inhibition of cycloxygenase, mucus secretion and mucosal blood flow may be involved. Aspirin also impair the quality of ulcer healing.

Risk Factors for Gastrointestinal Complications in Aspirin Users: Review of Clinical and Experimental Data

“…nitroglycerin protects against acidified aspirin-induced gastric mucosal injury in mice [88]. One recent study demonstrated that aspirin enhance the recurrence of gastric ulcer induced by acetic acid [89], suggesting that the acetic acid gastric ulcer model is suitable for assessing the effect of nitroglycerin on the enhancement of ulcer recurrence by aspirin.…”

Regulation of Gastric Acid Secretion by PKB/Akt2

“…At low expression levels of SGK1, as in the absence of glucocorticoids, the inhibitory effect appears to prevail. Beyond their effect on SGK1, glucocorticoids downregulate cycloxygenase [36,37], an effect similarly expected to enhance gastric acid secretion [36][37][38][39].…”

Regulation of basal gastric acid secretion by the glycogen synthase kinase GSK3

“…SGK1 has been shown to upregulate a wide variety of channels and transporters [43], including KCNQ1 [44][45][46]. Glucocorticoids exert further effects in gastric glands, such as the downregulation of cyclooxygenase [47,48], which is known to enhance gastric acid secretion [47][48][49][50]. At least in theory, these additional effects of glucocorticoids may modify PI3-kinase-dependent regulation of gastric acid secretion.…”