Gastroprotective effect of calealactone B: Lack of involvement of prostaglandins, nitric oxide and sulfhydryls.

Abstract

Hit, Lead & Candidate Discovery The gastroprotective effect of calealactone B, isolated from Calea urticifolia was assessed in an ethanol-induced model of gastric lesioning. The possible involvement of prostaglandins, nitric oxide (NO) and sulfhydryl groups in the mechanism of action of calealactone B was also assessed. Calealactone B inhibited ethanol-induced gastric injuries with a maximal effect (95.3 ± 2.6%) at 30 mg kg-1 . A similar value was obtained at 10 mg kg-1 (83.5 ± 7.7%). Meanwhile, the reference anti-ulcer drug, carbenoxolone, an 11β-hydroxysteroid dehydrogenase (11β-HSD) inhibitor administered at 30 mg kg-1 showed 63.5 ± 9.4% gastroprotection. Hence, calealactone B was more potent than carbenoxolone. Pretreatment with indomethacin, L-NAME or NEM did not reverse the effects of calealactone B, indicating that prostaglandins, NO and sulfhydryl compounds do not participate in its mechanism of action.