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The nitric oxide-cyclic GMP-K

Mohammad Amin Behmanesh1, Amin Rasekhian2, Forutan Kiani2

  • 1Department of Histology, School of Medicine, Dezful University of Medical Sciences, Dezful, Iran.

Alcohol (Fayetteville, N.Y.)
|June 9, 2023
PubMed
Summary

Montelukast, a leukotriene receptor antagonist, demonstrated gastroprotective effects against ethanol-induced gastric damage in rats. This protection involves the nitric oxide-cyclic guanosine monophosphate-ATP-sensitive potassium channel pathway.

Keywords:
NO-cGMP-K(ATP) channelethanolgastroprotectionmontelukastrat

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Area of Science:

  • Pharmacology
  • Gastroenterology
  • Cellular Signaling

Background:

  • Leukotrienes are lipid mediators implicated in ethanol-induced gastric damage.
  • Understanding the mechanisms of gastroprotection is crucial for developing effective treatments.

Purpose of the Study:

  • To evaluate the gastroprotective effect of montelukast, a leukotriene receptor antagonist.
  • To investigate the involvement of the nitric oxide (NO)-cyclic guanosine monophosphate (cGMP)-ATP-sensitive potassium channel (KATP) pathway in montelukast's action.

Main Methods:

  • Ethanol-induced gastric damage model in rats.
  • Administration of montelukast alone or in combination with agents modulating the NO-cGMP-KATP pathway (l-arginine, l-NAME, methylene blue, sildenafil, diazoxide, glibenclamide).
  • Assessment of macroscopic, microscopic, and pro-inflammatory cytokine (TNF-α, IL-1β) levels.

Main Results:

  • Montelukast significantly reduced ethanol-induced gastric lesions (macroscopic and microscopic) and pro-inflammatory cytokine levels.
  • Inhibition of nitric oxide synthase (NOS), guanylate cyclase, or KATP channels attenuated montelukast's protective effect.
  • Pretreatment with NO precursor, PDE-5 inhibitor, or KATP channel opener enhanced gastroprotection.

Conclusions:

  • Montelukast exhibits significant gastroprotective effects against ethanol-induced gastric injury in rats.
  • The gastroprotective mechanism of montelukast is, at least partly, mediated by the NO-cGMP-KATP channel pathway.