Acute effects of the cys-leukotriene-1 receptor antagonist, montelukast, on experimental colitis in rats

Holma, Reetta; Salmenperä, Pertteli; Riutta, Asko; Virtanen, Ismo; Korpela, Riitta; Vapaatalo, Heikki

doi:10.1016/s0014-2999(01)01330-9

Cited by 58 publications

(34 citation statements)

References 51 publications

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“…Studies have shown conflicting results regarding the effect of leukotriene blockade on the expression of COX-2 [21][22][23] . These conflicting data may be explained by the "shunt" effect between cyclooxygenase and leukotriene pathways 9 .…”

Section: ■ Discussionmentioning

confidence: 99%

Role of the route of leukotrienes in an experimental model of oral mucositis induced by 5-fluorouracil

Silva

Leitão²,

Brito³

et al. 2017

Acta Cir. Bras.

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Role of the route of leukotrienes in an experimental model of oral mucositis induced by 5-fluorouracil 1 AbstractPurpose: To investigate the participation of cysteinyl leukotrienes in the pathophysiology of oral mucositis. Methods: Oral mucositis was induced in hamsters using 5-fluorouracil (5-FU; 60 and 40 mg/ kg; i.p., on days 1 and 2, respectively, and with excoriations in jugal mucosa on day 4). Montelukast (10, 20, or 40 mg/kg/d; gavage), MK886 (3 mg/kg/d, i.p.), or saline or celecoxib (7.5 mg/kg/d; i.p.) was administered 1 h prior to 5-FU and daily, until the fourth (MK886) or tenth day, when the animals were euthanized and their jugal mucosa was collected for macroscopic, histopathological, and immunohistochemical evaluation. Results: Neither montelukast nor MK-886 prevented the oral mucositis induced by 5-FU, as observed by histopathological evaluation. In addition, we did not find significant differences in the expression of inducible nitric oxide synthase-2, cyclooxygenase-2, or interleukin (IL)-1β between the experimental and control groups. However, we did observe a significant decrease in tumor necrosis factor (TNF)-α expression for all doses of montelukast; we also observed a significant decrease in IL-10 with 40 mg/kg/d and MK 886. Conclusions: Cysteinyl leukotrienes do not play an important role in experimental oral mucositis induced by 5-FU. There is a modulating action specifically on TNF-α.

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Section: ■ Discussionmentioning

confidence: 99%

Role of the route of leukotrienes in an experimental model of oral mucositis induced by 5-fluorouracil

Silva

Leitão²,

Brito³

et al. 2017

Acta Cir. Bras.

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“…The elimination of ROS has been shown to be beneficial in treating ischemia-reperfusion injury. 16,25,26 The ROS are difficult to quantify directly in tissue because of their high reactivity and short half-life. Malondialdehyde, Testes ischemia a stable end-product of lipid peroxidation generated by ROS, is usually used as a good indicator of the degree of lipid peroxidation.…”

Section: Discussionmentioning

confidence: 99%

“…In our experiment, we determined the malondialdehyde (MDA) level, an end product of lipid peroxidation; 11 the glutathione (GSH) level, a key antioxidant; 12 Testes ischemia and the tissue-associated MPO activity, as indirect evidence of neutrophil infiltration. 13 Anti-leukotriene agents have been shown to be effective to protect against injury in several inflammatory models in rats, such as in ethanol-induced gastric mucosal damage, 14 colitis 15,16 burn-and sepsis-induced multiorgan damage 17,18 and renal I-R injury. 19 Based on these findings, in the present study, we examined the protective effect of the selective LTD 4 receptor antagonist, montelukast (MK-0476), on histologic damage induced by testes I-R in rats.…”

Section: Introductionmentioning

confidence: 99%

Montelukast protects against testes ischemia/reperfusion injury in rats

Öztürk

Gideroğlu

et al. 2013

CUAJ

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Introduction: In this study, we investigate the effect of montelukast on histologic damage induced by testicular torsion-detorsion in rats. Methods: Twenty-one male Sprague-Dawley rats were separated into 3 groups, each containing 7 rats. A sham operation was performed in group 1 (control). In group 2 (ischemia-reperfusion [I-R]/untreated), 1-hour detorsion of the testis was performed after 6 hours of unilateral testicular torsion. In group 3 (I-R/dextroamphetamine), after performing the same surgical procedures as in group 2, montelukast was given intraperitoneally. In all experimental rats, ipsilateral orchiectomies were performed for histological examination and tissue malondialdehyde (MDA), glutathione and myeloperoxidase assays. Results: Montelukast treatment significantly decreased the I-Rinduced elevation in testes tissue MDA and glutathione levels were found to be preserved. The level of myeloperoxidase (MPO) activity was significantly increased in the testes tissue of the I-R/untreated group. However, in I-R/montelukast treatment group significantly decreased testes tissue MPO level. Histopathologically, the in the group 2 rats, edema, congestion, hemorrhage between seminiferous tubules and necrosis of the germinal cells were predominant features in sections. However, most of the specimens in the montelukast treated group 3 showed grades-I and II injury. Additionally, the testicular injury score was lower in group 3 rats compared with group 2. Conclusion: The current findings demonstrate that the montelukast decreased the severity of testicular injury by reversing the oxidative effects of testes I-R. RésuméIntroduction : Dans cette étude, nous examinons l'effet du montélukast sur les lésions tissulaires provoquées par torsion-détorsion testiculaire chez le rat. Méthodologie : Vingt-et-un rats Sprague-Dawley mâles ont été répartis en trois groupes de 7 rats. Une opération fictive a été réalisée dans le groupe 1 (groupe témoin). Dans le groupe 2 (ischémie-reperfusion / non traité), une détorsion testiculaire d'une heure a été réalisée après 6 heures de torsion testiculaire unilatérale. Dans le groupe 3 (ischémie-reperfusion / dextroamphét-amine), on a administré du montélukast par voie intrapéritonéale après les mêmes interventions chirurgicales que pour le groupe 2. Chez tous les rats, une orchidectomie homolatérale a été effectuée en vue d'un examen histologique et de mesures du malonaldéhyde, du glutathion et de la myéloperoxidase dans les tissus. Résultats :Le traitement par montélukast a significativement réduit l'élévation dans les tissus testiculaires provoquée par l'ischémie-reperfusion, mais les taux de malonaldéhyde et de glutathion sont demeurés les mêmes. Le niveau d'activité de la myéloperoxidase (MPO) a significativement augmenté dans les tissus testiculaires du groupe ayant subi l'ischémie-reperfusion sans traitement subséquent. Cependant, dans le groupe ayant subi l'ischémie-reperfusion avec traitement par montélukast, le taux de MPO dans les tissus testiculaires avait significativ...

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“…In the present study, we observed that CysLTs content in the small intestinal mucosa was signifi cantly increased after administration of indomethacin. Holma et al (2001) and Kim et al (1995) reported that colonic CysLTs content was markedly elevated in the rats treated with trinitrobenzene sulfonic acid (TNBS) as well as the patients with active Crohn's diseases. Mahgoub et al (2003) reported that zafi rlukast, a CysLT1 receptor antagonist, prevented acetic acid-induced colon lesions, supporting the involvement of CysLTs in the pathogenesis of colonic ulceration.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of pranlukast, a cysteinyl-leukotriene receptor 1 antagonist, on indomethacin-induced small intestinal damage in rats

et al. 2007

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We examined the effect of pranlukast, the receptor antagonist of the cysteinyl leukotrienes (CysLTs; LTC(4), LTD4 and LTE4), on indomethacin-induced small intestinal lesions in rats. Animals non-fasted were given indomethacin (10 mg/kg) s.c., and killed 24 hr later. Pranlukast (1-10 mg/kg) was given p.o. twice, 30 min before and 6 hr after the administration of indomethacin. A single s.c. administration of indomethacin provoked multiple haemorrhagic lesions in the small intestine, mainly in the jejunum and ileum. This treatment also caused an increase in MPO activity, microvascular permeability, and enterobacterial counts in the mucosa. Pretreatment of the animals with pranlukast (1-10 mg/kg) dose-dependently reduced the severity of these lesions and improved the patho-physiological alterations occurred after indomethacin treatment. Although indomethacin increased intestinal motility and decreased mucus secretion, the events being responsible for bacterial invasion, these changes were not significantly affected by pranlukast. These results showed that pranlukast prevents indomethacin-induced small intestinal lesions, probably through its inhibitory action, primarily on bacterial invasion and secondly on neutrophil migration as well as vascular permeability, and suggest the importance of CysLTs in the pathogenic mechanism of this lesion model.

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Acute effects of the cys-leukotriene-1 receptor antagonist, montelukast, on experimental colitis in rats

Cited by 58 publications

References 51 publications

Role of the route of leukotrienes in an experimental model of oral mucositis induced by 5-fluorouracil

Role of the route of leukotrienes in an experimental model of oral mucositis induced by 5-fluorouracil

Montelukast protects against testes ischemia/reperfusion injury in rats

Protective effect of pranlukast, a cysteinyl-leukotriene receptor 1 antagonist, on indomethacin-induced small intestinal damage in rats

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