Montelukast ameliorates kidney function and urinary bladder sensitivity in experimentally induced renal dysfunction in rats

Suddеk, Ghada M.

doi:10.1111/j.1472-8206.2011.00996.x

Cited by 26 publications

(17 citation statements)

References 21 publications

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“…MNT had also been demonstrated to increase the level of GSH in rats with indomethacin-induced gastric ulcer, 12 gentamicininduced nephrotoxicity and oxidative damage, 32 and those with cisplatin-induced nephrotoxicity. 33 Our results confirm that the inhibition of tissue lipid peroxidation along with replenishment of GSH content by MNT implies that the compound is beneficial in maintaining oxidant-antioxidant balance. Although, MNT does not have a known effect to stimulate GSH biosynthesis, it seems plausible that it can improve the antioxidant defense system by inhibiting the lipid peroxidation reaction, thus, mitigating the consumption of GSH.…”

Section: Discussionsupporting

confidence: 84%

Montelukast attenuates lipopolysaccharide-induced cardiac injury in rats

et al. 2015

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This study investigates the possible protective effects of montelukast (MNT) against lipopolysaccharide (LPS)-induced cardiac injury, in comparison to dexamethasone (DEX), a standard anti-inflammatory. Male Sprague Dawley rats (160–180 g) were assigned to five groups ( n = 8/group): (1) control; (2) LPS (10 mg/kg, intraperitoneal (i.p.)); (3) LPS + MNT (10 mg/kg, per os (p.o.)); (4) LPS + MNT (20 mg/kg, p.o.); and (5) LPS + DEX (1 mg/kg, i.p.). Twenty-four hours after LPS injection, heart/body weight (BW) ratio and percent survival of rats were determined. Serum total protein, creatine kinase muscle/brain (CK-MB), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) activities were measured. Heart samples were taken for histological assessment and for determination of malondialdehyde (MDA) and glutathione (GSH) contents. Cardiac tumor necrosis factor α (TNF-α) expression was evaluated immunohistochemically. LPS significantly increased heart/BW ratio, serum CK-MB, ALP, and LDH activities and decreased percent survival and serum total protein levels. MDA content increased in heart tissues with a concomitant reduction in GSH content. Immunohistochemical staining of heart specimens from LPS-treated rats revealed high expression of TNF-α. MNT significantly reduced percent mortality and suppressed the release of inflammatory and oxidative stress markers when compared with LPS group. Additionally, MNT effectively preserved tissue morphology as evidenced by histological evaluation. MNT (20 mg/kg) was more effective in alleviating LPS-induced heart injury when compared with both MNT (10 mg/kg) and DEX (1 mg/kg), as evidenced by decrease in positive staining by TNF-α immunohistochemically, decrease MDA, and increase GSH content in heart tissue. This study demonstrates that MNT might have cardioprotective effects against the inflammatory process during endotoxemia. This effect can be attributed to its antioxidant and/or anti-inflammatory properties.

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Section: Discussionsupporting

confidence: 84%

Montelukast attenuates lipopolysaccharide-induced cardiac injury in rats

et al. 2015

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“…Flavocoxid action may also be mediated by its inhibitory effect on 5-LOX-mediated LT production. Similarly, in the study of Suddek (2013), montelukast, a leukotriene receptor antagonist, has been found to antagonize the constrictor effect of ACh on the urinary bladder and protect the urinary bladder from hypersensitivity to ACh induced by treatment with cisplatin, another nephrotoxic agent.…”

Section: Discussionmentioning

confidence: 96%

Flavocoxid attenuates gentamicin-induced nephrotoxicity in rats

El‐Kashef

El-Kenawi

Suddеk

et al. 2015

Naunyn-Schmiedeberg's Arch Pharmacol

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Gentamicin is a widely used antibiotic against serious and life-threatening infections; however, its usefulness is limited by the development of nephrotoxicity. The present study was designed to determine whether flavocoxid has a protective effect against gentamicin-induced nephrotoxicity in rats. For this purpose, we quantitatively evaluated gentamicin-induced renal structural and functional alterations using histopathological and biochemical approaches. Furthermore, the effect of flavocoxid on gentamicin induced hypersensitivity of urinary bladder rings to acetylcholine (ACh) was determined. Twenty-four male Wistar albino rats were randomly divided into three groups, namely control, gentamicin (100 mg/kg, i.p.) and gentamicin plus flavocoxid (20 mg/kg, orally). At the end of the study, all rats were sacrificed and then blood, urine samples and kidneys were collected for further analysis. Gentamicin administration caused a severe nephrotoxicity which was evidenced by an elevated renal somatic index (RSI), serum creatinine, blood urea nitrogen, serum lactate dehydrogenase, and protein in urine with a concomitant reduction in serum albumin and normalized creatinine clearance value as compared with the controls. Moreover, a significant increase in renal contents of malondialdehyde, myeloperoxidase, and tumor necrosis factor-alpha with a significant decrease in renal reduced glutathione and superoxide dismutase activities was detected upon gentamicin administration together with increasing the sensitivity of isolated urinary bladder rings to ACh. Exposure to gentamicin induced necrosis of renal tubular epithelial cells. Flavocoxid protected kidney tissue against the oxidative damage and the nephrotoxic effect caused by gentamicin treatment. In addition, flavocoxid significantly reduced the responses of isolated bladder rings to ACh. The results from our study indicate that flavocoxid supplement attenuates gentamicin-induced renal injury via the amelioration of oxidative stress and inflammation of renal tubular cells.

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“…GSH is one of the endogenous antioxidant against a number of noxious stimuli including free oxygen radicals and several reports indicate that reduction of cellular GSH is accompanied by lipid peroxidation. It was shown that montelukast suppresses the release of oxidative stress markers and enhances enzymatic antioxidant activities in urinary bladder in spinal cord injury induced secondary degeneration (34) and kidney in cisplatin induced renal disfunction (35). In this study, the MDA level was significantly increased and GSH level was significantly decreased by WAS exposure.…”

Section: Discussionmentioning

confidence: 46%

Protective Effects of Montelukast Against Stress-Induced Degeneration of the Urinary Bladder

Dülger¹,

Canillioglu²,

Çetınel³

et al. 2017

Clin Exp Health Sci

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Objective: The aim of the study was to investigate the role of montelukast (ML), a cysteinyl leukotriene-1 receptor antagonist, on the water avoidance stress (WAS)induced degeneration of the rat urinary bladder mucosa. Methods: In WAS group, rats were exposed to WAS two hours daily for five days. In WAS+ML group, rats were administered ML (10 mg/kg; i.p.;) following every WAS exposure for 5 days. In control group, rats were injected vehicle solution only. The urinary bladder was evaluated for general morphology at light microscope. Mast cell activation and uroplakin distribution were assessed with immunohistochemistry. Glycosaminoglycan (GAG) distribution and urothelial permeability were observed using ruthenium red (RR) staining techniques in transmission electron microscope and luminal urothelial cells were observed with scanning electron microscope. Tissue malondialdehyde (MDA) and gluthatione (GSH) levels were also analysed. Results: Irregular GAG layer and uroplakin distribution, penetration of RR in the intercellular spaces and dilated tight junctions in urothelial layer, increase in inflammatory cell infiltration, in number of both granulated and activated mast cells, and were observed in the WAS group. The MDA level was increased, and GSH level was decreased significantly in urinary bladder in the WAS group in comparison with the control group. Quite regular GAG layer, uroplakin distribution and tight junctions in most regions, decrease in inflammatory cell infiltration and both of activated and granulated mast cells in the mucosa, were observed in WAS+ML group. Moreover, significant decrease in MDA and increase in GSH levels were observed in this group. Conclusion: Montelukast appears to exert a protective activity in WAS induced urinary bladder injury by inhibiting inflammatory and oxidative activity.

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Montelukast ameliorates kidney function and urinary bladder sensitivity in experimentally induced renal dysfunction in rats

Abstract: Montelukast may be a beneficial remedy for cisplatin-induced renal dysfunction.

Cited by 26 publications

References 21 publications

Montelukast attenuates lipopolysaccharide-induced cardiac injury in rats

Montelukast attenuates lipopolysaccharide-induced cardiac injury in rats

Flavocoxid attenuates gentamicin-induced nephrotoxicity in rats

Protective Effects of Montelukast Against Stress-Induced Degeneration of the Urinary Bladder

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