Adenosine Protects Against Indomethacin-Induced Gastric Damage in Rats (original) (raw)

1998, Digestive Diseases and Sciences

This study examines the putativegastroprotective effect of adenosine onindomethacininduced gastric lesions and the possiblemechanisms involved. After 24 hr of starvation, the ratswere treated either with indomethacin (Indo; 25 mg/kg,subcutaneously) alone or adenosine + Indo (Ado; 7.5mg/kg, subcutaneously, three times a day), or thevehicle (5% NaHCO3, subcutaneously). Thelength of hemorrhagic lesions in the stomachs was expressed as the lesionindex. The tissue-associated

A 1 AND A 2 adenosine receptors mediate opposite effects on nsaid-induced gastric ulcers in the rat

Inflammopharmacology, 1995

Some adenosine modulators can modify stress- and ethanol-induced ulcers. However, little is known about their effects on NSAID-induced gastric ulcers. Our studies show that cyclopentyladenosine (CPA), an A1 selective receptor agonist, produced exacerbation of the NSAID-induced gastric lesion (100% at 10 mg/kg p.o.). CPA administered alone also demonstrated ulcerogenic capacity. PD-125944 (DPMA) and CGS 21680, A2a selective agonists, protected gastric mucosa from NSAID-induced damage with ED50 of 4.4 and 1.2 mg/kg p.o. respectively. The effect of DPMA was reversed by 8-(3-chlorostyryl) caffeine (CSC), an A2A antagonist, with an ID50 of 9 mg/kg i.p. The adenosine uptake blocker S-(4-nitrobenzyl)-6-thioinosine (NBTT; 1 mg/kg i.p.) reversed the damage with maximum inhibition of 50-60%. This response was reversed by CSC (10 mg/kg i.p.) but not by 8-cyclopentyl-l,3-dipropylxanthine (5 mg/kg i.p.), an A1 receptor antagonist. These data suggest that selective activation of A2 adenosine receptors completely prevents indomethacin-induced gastric ulcers. However, selective stimulation of A1 receptors causes both direct gastric damage and enhances that induced by NSAIDs. Therefore, an increase in endogenous adenosine produces partial inhibition of the injury, suggesting a predominant role for A2 receptors in the regulation of gastric mucosa integrity.

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