Gastroprotective effects of irsogladine maleate on ethanol/hydrochloric acid induced gastric ulcers in mice

Abstract

Background/Aims This study was conducted to investigate the inhibitory effect of irsogladine maleate (IM) on gastric ulcers induced by ethanol and hydrochloric acid (HCl). Methods Mice were pretreated with IM for 1 hours before ulcer induction. Gastric ulcers were induced by oral administration of an ethanol/HCl mixture. To clarify the action mechanism of IM, the roles of 3ʹ5ʹ-cyclic adenosine monophosphate (cAMP), nitric oxide (NO), adenosine triphosphate-sensitive potassium (KATP) channels, prostaglandins and transient receptor potential cation channel subfamily V member 1 (TRPV1) were investigated, and lipid peroxidation in the stomach of IM-treated and -untreated animals was also measured. Results IM significantly reduced the extent of ethanol/HCl mixture-induced gastric ulceration. It exhibited dose-related gastroprotection against the ethanol/HCl-induced lesions, while pretreatment with glibenclamide but not N(ω)-nitro- L-arginine methyl ester, reversed this action. While pretreatment with the TRPV1 antagonist capsazepine failed to effectively block the gastroprotective effect of IM, the non-selective cyclooxygenase inhibitor indomethacin almost abolished it. IM also decreased the level of thiobarbituric acid reactive substances. Conclusions We concluded that IM exhibited significant gastroprotective effects in an ethanol/HCl-induced ulcer model, which appear to be mediated, at least in part, by NO, cAMP, endogenous prostaglandins, KATP channel opening, activation of TRPV1 channels, and antioxidant properties

Keywords

• irsoglandine maleate
• anti-ulcer
• stomach ulcer