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Mechanisms of gastroprotective effect of eugenol in indomethacin‐induced ulcer in rats
Author(s) -
Morsy Mohamed A.,
Fouad Amr A.
Publication year - 2008
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.2502
Subject(s) - eugenol , glibenclamide , pharmacology , nitric oxide , malondialdehyde , chemistry , pepsin , indometacin , stomach , oral administration , channel blocker , antioxidant , medicine , biochemistry , endocrinology , enzyme inhibitor , prostaglandin endoperoxide synthase , enzyme , organic chemistry , in vitro , calcium , diabetes mellitus
Possible mechanisms underlying the gastroprotective effect of eugenol against indomethacin‐induced ulcer in rats were investigated. Pyloric ligation was performed for collection of gastric juice, and gastric ulceration was induced by a single intraperitoneal (i.p.) injection of indomethacin (30 mg/kg). Pretreatment with a single dose of eugenol (100 mg/kg, orally), 1 h before indomethacin administration caused significant reductions in gastric mucosal lesions, gastric acid outputs and pepsin activity associated with a significant increase in mucin concentration. Additionally, eugenol significantly attenuated the elevations in gastric mucosal malondialdehyde and total nitrite, and the decrease in reduced glutathione observed with indomethacin. The protective effect afforded by eugenol was significantly inhibited by prior administration of glibenclamide, the ATP‐sensitive potassium (K ATP ) channel blocker, but not by prior use of ruthenium red, the transient receptor potential vanilloid 1 (TRPV1) antagonist. The results indicate that the anti‐ulcer effect of eugenol is mediated by opening of K ATP channels, scavenging free radicals, decreasing acid‐pepsin secretion, increasing mucin production, and preventing the deleterious rise in nitric oxide level. Copyright © 2008 John Wiley & Sons, Ltd.