Gastroprotective effect of leukotriene receptor blocker montelukast in alendronat-induced lesions of the rat gastric mucosa

Şener, Göksel; Kapucu, Caner; Çetınel, Şule; Çikler, Esra; Ayanoğlu-Dülger, Gül

doi:10.1016/j.plefa.2004.04.005

Cited by 37 publications

(24 citation statements)

References 42 publications

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“…However, while montelukast, lansoprazole, famotidine, and ranitidine reduced the development of indomethacin-induced gastric damage, this reduction occurred at a greater magnitude for montelukast, famotidine, and lansoprazole than for ranitidine, an H 2 -receptor blocker (Table 1). Sener et al (36) have shown the gastroprotective effects of montelukast in alendronateinduced lesions of the rat gastric mucosa. They reported that the gastroprotective effect of montelukast is related to its effects on the antioxidants and MPO activity.…”

Section: Discussionmentioning

confidence: 99%

Gastroprotective and Antioxidant Effects of Montelukast on Indomethacin-Induced Gastric Ulcer in Rats

Dengiz¹,

Odabaşoğlu

Halıcı

et al. 2007

J Pharmacol Sci

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Abstract. Montelukast, a selective reversible cysteinyl leukotriene D 4 -receptor (LTD 4 receptor) antagonist, is used in the treatment of asthma. We have investigated alterations in the glutathione (GSH) and activity levels of antioxidative enzymes [superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), and glutathione reductase (GR)] and myeloperoxidase (MPO), as markers of the ulceration process following oral administration of montelukast, lansoprazole, famotidine, and ranitidine, respectively, in rats with indomethacin-induced ulcers. In the present study, we found that 1) montelukast, lansoprazole, famotidine, and ranitidine all reduced the development of indomethacin-induced gastric damage, with this reduction occurring at a greater magnitude for montelukast, famotidine, and lansoprazole than for ranitidine; 2) montelukast and ranitidine both alleviated increases in the activity levels of CAT and GST enzymes resulting from gastric injury; 3) montelukast and ranitidine both ameliorated depressions in the GSH and activity levels of SOD and GR enzymes caused by indomethacin administration; and 4) all doses of montelukast, lansoprazole, and ranitidine decreased amplification of MPO activity resulting from induced gastric injuries. These results suggest that the gastroprotective effects of montelukast on indomethacin-induced ulcerations can be attributed to its ameliorating effect on oxidative damage and MPO activity.

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Section: Discussionmentioning

confidence: 99%

Gastroprotective and Antioxidant Effects of Montelukast on Indomethacin-Induced Gastric Ulcer in Rats

Dengiz¹,

Odabaşoğlu

Halıcı

et al. 2007

J Pharmacol Sci

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“…This effect can induce gastric erosions and apoptosis by DNA fragmentation [38,39]. Also, it has been suggested that oxygen-derived free radicals may contribute to ALD-induced gastric mucosal lesions [15,40,41]. However, the mechanism by which ALD generates ROS to cause mucosal damage has not yet been clarified.…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Simvastatin Against Alendronate-Induced Gastric Mucosal Injury in Rats

Carvalho

Silva

et al. 2015

Dig Dis Sci

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“…The anatomical distribution of both the gastric ulcers and esophageal damage is consistent with the topical irritant effect of bisphosphonates, but its clinical significance is still uncertain (Graham 2002). We have previously investigated the mechanism(s) underlying the gastrointestinal damaging property of chronic treatment with ALD, and suggested that ALD causes gastric damage by a direct effect on the mucosa, resulting in a direct oxidative damage, and also by an indirect oxidative damage through induction of neutrophil infiltration (Sener et al 2005). It has been previously shown that at pH<2, ALD sodium is converted to its acid form (Peter et al 1998), which is known to be more irritating than the sodium salt.…”

Section: Discussionmentioning

confidence: 99%

“…Based on our previous studies (Sener et al 2004(Sener et al , 2005, ALD was given by gavage (20 mg/kg) once a day for 4 days following overnight fasting periods. Either ghrelin (10 ng/kg per day) or saline was given i.p.…”

Section: Animalsmentioning

confidence: 99%

Ghrelin against alendronate-induced gastric damage in rats

İşeri

Şener²,

Yüksel³

et al. 2005

Journal of Endocrinology

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Alendronate sodium, a primary amino bisphosphonate, is widely used in the treatment of various diseases that are associated with bone resorption, such as postmenopausal osteoporosis and Paget's disease of bone. Although the adverse effects of biphosphonates on the gastrointestinal system have been demonstrated in experimental and clinical studies, the exact mechanisms underlying this damage are not clear yet. Ghrelin, a 28 amino acid peptide produced predominantly by the stomach, was shown to exert a potent protective action on the stomach of rats exposed to ethanol or stress.Our objective was to evaluate the possible antioxidant and anti-inflammatory effects of ghrelin against alendronate-induced gastric damage. Wistar albino rats were administered alendronate (20 mg/kg) by gavage for 4 days, along with either ghrelin (10 ng/kg per day) or saline given i.p. After decapitation, stomach tissues were removed for the determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and tissue collagen content, while the extent of tissue damage was analyzed microscopically. Formation of reactive oxygen species was determined by chemiluminesence using a luminol probe in fresh gastric tissues. Serum tumor necrosis factor (TNF-) and lactate dehydrogenase levels were assessed in trunk blood.Oral administration of alendronate-induced significant gastric damage, accompanied by increased MPO activity, collagen content, MDA and luminol levels (P<0·01-P<0·001), while tissue GSH was decreased (P<0·01). On the other hand, ghrelin treatment reversed these alterations (P<0·05-P<0·001) as well as elevating serum TNF-levels significantly (P<0·001).The findings of the present study suggest that alendronate induces oxidative gastric damage by a local irritant effect, and ghrelin ameliorates this damage by its possible antioxidant and anti-inflammatory properties.

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Gastroprotective effect of leukotriene receptor blocker montelukast in alendronat-induced lesions of the rat gastric mucosa

Cited by 37 publications

References 42 publications

Gastroprotective and Antioxidant Effects of Montelukast on Indomethacin-Induced Gastric Ulcer in Rats

Gastroprotective and Antioxidant Effects of Montelukast on Indomethacin-Induced Gastric Ulcer in Rats

Protective Effects of Simvastatin Against Alendronate-Induced Gastric Mucosal Injury in Rats

Ghrelin against alendronate-induced gastric damage in rats

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