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Gastroprotective effect of calealactone B: Lack of involvement of prostaglandins, nitric oxide and sulfhydryls
Author(s) -
SánchezMendoza María Elena,
LópezLorenzo Yaraset,
MatusMeza AudifásSalvador,
Arrieta Jesús
Publication year - 2018
Publication title -
drug development research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.582
H-Index - 60
eISSN - 1098-2299
pISSN - 0272-4391
DOI - 10.1002/ddr.21415
Subject(s) - carbenoxolone , nitric oxide , chemistry , pharmacology , mechanism of action , ethanol , prostaglandin e , biochemistry , in vitro , medicine , intracellular , organic chemistry , gap junction
Hit, Lead & Candidate DiscoveryThe 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.