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Carbenoxolone gastroprotective mechanism: participation of nitric oxide/ c GMP/K ATP pathway in ethanol‐induced gastric injury in the rat
Author(s) -
ChávezPiña Aracely Evangelina,
TapiaÁlvarez Gabriela Rubí,
ReyesRamínrez Adelfo,
Navarrete Andrés
Publication year - 2011
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1111/j.1472-8206.2010.00897.x
Subject(s) - carbenoxolone , nitric oxide , glibenclamide , pharmacology , chemistry , ethanol , mechanism of action , medicine , endocrinology , gap junction , biochemistry , in vitro , diabetes mellitus , intracellular
Carbenoxolone, a semi‐synthetic triterpenoid, exhibits gastroprotective activity related to the participation of nitric oxide (NO); however, the complete NO/ c GMP/K ATP channels pathway for carbenoxolone is unknown. Therefore the aim of this study was to examine the NO/ c GMP/K ATP channels pathway as the gastroprotective mechanism of carbenoxolone in the ethanol‐induced gastric injury model in the rat. Oral administration of carbenoxolone (30 mg/kg, p.o.) exhibited gastroprotective effect against ethanol‐induced gastric injury in rats. Pretreatment with N G ‐nitro‐ l ‐arginine methyl ester ( L ‐NAME, 70 mg/kg, i.p.); 1H‐[1,2,4]oxadiazolo[4,3‐a]quinoxaline‐1‐one (ODQ, guanylate cyclase inhibitor, 10 mg/kg, i.p.); or glibenclamide (K ATP channels inhibitor, 1 mg/kg, i.p.) reversed the gastroprotective effect of carbenoxolone for ethanol‐induced gastric injury. Furthermore, gastric prostaglandins and NO levels increased after carbenoxolone administration in ethanol‐induced gastric injury in rats. In conclusion, our results suggest that the increase of NO levels in gastric tissue after pretreatment with carbenoxolone activates the NO/ c GMP/K ATP channels pathway, the principal gastroprotective mechanism of carbenoxolone.