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Gastroprotection of (‐)‐α‐bisabolol on acute gastric mucosal lesions in mice: the possible involved pharmacological mechanisms
Author(s) -
Moura Rocha Nayrton Flávio,
Venâncio Edith Teles,
Moura Brinell Arcanjo,
Gomes Silva Maria Izabel,
Aquino Neto Manoel Rufino,
Vasconcelos Rios Emiliano Ricardo,
De Sousa Damião Pergentino,
Mendes Vasconcelos Silvânia Maria,
De França Fonteles Marta Maria,
De Sousa Francisca Cléa Florenço
Publication year - 2010
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.1472-8206.2009.00726.x
Subject(s) - pharmacology , ethanol , chemistry , oral administration , glutathione , capsaicin , gastric mucosa , bioavailability , glibenclamide , mechanism of action , stomach , medicine , biochemistry , endocrinology , receptor , in vitro , diabetes mellitus , enzyme
(‐)‐α‐Bisabolol is an unsaturated, optically active sesquiterpene alcohol obtained by the direct distillation essential oil from plants such as Vanillosmopsis erythropappa and Matricaria chamomilla . (‐)‐α‐Bisabolol has generated considerable economic interest, since it possesses a delicate floral odor and has been shown to have anti‐septic and anti‐inflammatory activity . The aim of this work was to evaluate the gastroprotective action of (‐)‐α‐bisabolol on ethanol and indomethacin‐induced ulcer models in mice, and further investigate the pharmacological mechanisms involved in this action. The oral administration of (‐)‐α‐bisabolol 100 and 200 mg/kg was able to protect the gastric mucosa from ethanol (0.2 mL/animal p.o.) and indomethacin‐induced ulcer (20 mg/kg p.o.). Administration of l ‐NAME (10 mg/kg i.p.), glibenclamide (10 mg/kg i.p.) or indomethacin (10 mg/kg p.o.) was not able to revert the gastroprotection promoted by (‐)‐α‐bisabolol 200 mg/kg on the ethanol‐induced ulcer. Dosage of gastric reduced glutathione (GSH) levels showed that ethanol and indomethacin reduced the content of non‐protein sulfhydryl (NP‐SH) groups, while (‐)‐α‐bisabolol significantly decreased the reduction of these levels on ulcer‐induced mice, but not in mice without ulcer. In conclusion, gastroprotective effect on ethanol and indomethacin‐induced ulcer promoted by (‐)‐α‐bisabolol may be associated with an increase of gastric sulfydryl groups bioavailability leading to a reduction of gastric oxidative injury induced by ethanol and indomethacin.