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The effect of montelukast, a leukotriene receptor antagonist, on the acetic acid-induced model of colitis in rats: Involvement of NO-cGMP-KATP channels pathway
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Behnam GhorbanzadehGhorbanzadeh   , Mohammad Amin Behmanesh , Roya Mahmoudinejad , Mehdi Zamaniyan , Shadi Ekhtiar , Yousef Paridar |
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Abstract: (287 Views) |
Introduction: Inflammatory bowel disease is a chronic autoimmune disorder that may involve the entire gastrointestinal tract. The leukotrienes have a role as mediators in the pathophysiology of colitis. We investigated the effect of a leukotriene receptor antagonist, montelukast, and also the role of the NO-cGMP-KATP channel pathway in acetic acid-induced colitis.
Methods and Materials: Rectal administration of acetic acid (4%) was used for the induction of colitis in rats. To investigate our hypothesis, the rats were intraperitoneally pre-treated with L-NAME (NOS inhibitor), L-arginine, sildenafil, methylene blue, glibenclamide, or diazoxide 15 min before treatment with montelukast (5–20 mg/kg, i. p.), for three consecutive days. Then, microscopic, macroscopic, and inflammatory parameters were evaluated.
Results: Montelukast reduced the microscopic and macroscopic damage induced by acetic acid. Montelukast also reduced the level of IL-1β and TNF-α. We also showed that the effects of montelukast were significantly attenuated by L-NAME, methylene blue (guanylate cyclase inhibitor), and an ATP-sensitive potassium channel blocker (glibenclamide). Also, the administration of L-arginine, sildenafil, and diazoxide before montelukast produced a protective effect.
Conclusions: The pathway of the NO-cGMP-KATP channel is involved in the protective effect of montelukast in acetic acid-induced colonic tissue damage.
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| Keywords: Montelukast, Nitric oxide, cGMP, KATP channels, Inflammatory bowel |
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Full-Text [PDF 330 kb]
(44 Downloads)
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Type of Study: Research |
Subject:
General
Received: 2023/12/4 | Accepted: 2023/08/23 | Published: 2023/08/23
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