arachidonyl-2-chloroethylamide and Stomach-Ulcer

The involvement of nitric oxide in the gastroprotective effect of ACEA (arachidonyl-2-chloroethylamide), a selective cannabinoid CB1 receptor agonist, on aspirin-induced gastric ulceration was studied in rats. ACEA (3 mg/kg i.p.) significantly reduced gastric ulcer formation. The gastroprotection of ACEA was attenuated by pretreatment with L-NAME (25 and 50 mg/kg i.p.), a nitric oxide synthase inhibitor. The combination of L-arginine (300 mg/kg i.v.), a precursor of nitric oxide with L-NAME (50 mg/kg i.p.) reversed the protective activity of ACEA (3 mg/kg i.p.). These results suggest that endogenous nitric oxide may be involved in the protective effect of ACEA.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Anti-Ulcer Agents; Arachidonic Acids; Arginine; Aspirin; Enzyme Inhibitors; Female; Male; NG-Nitroarginine Methyl Ester; Nitric Oxide; Nitric Oxide Synthase; Rats; Rats, Wistar; Receptor, Cannabinoid, CB1; Stomach Ulcer

The effect of a selective cannabinoid CB1 receptor agonist, ACEA (arachidonyl-2-chloroethylamide) in an aspirin-induced ulcer model was studied in rats. ACEA (1.25-5 mg/kg i.p.) significantly reduced gastric ulcer formation to 24, 21 and 0.6% respectively. These results confirm the cytoprotective effect of CB1 receptor agonists and suggest that the endocannabinoid system might be the target for a novel class of anti-ulcer drugs.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Anti-Ulcer Agents; Arachidonic Acids; Aspirin; Dose-Response Relationship, Drug; Gastric Mucosa; Ranitidine; Rats; Receptor, Cannabinoid, CB1; Stomach Ulcer