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

Korean Journal of Internal Medicine 2021년 36권 1호 p.67 ~ 75
권성춘, 김지훈,
소속 상세정보
권성춘 ( Kwon Seong-Chun ) - Catholic Kwandong University College of Medicine Department of Physiology
김지훈 ( Kim Ji-Hoon ) - University of Ulsan College of Medicine Gangneung Asan Hospital Department of Surgery

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 3?5?-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

키워드

Irsoglandine maleate; Anti-ulcer; Stomach ulcer

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