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Montelukast protects against renal ischemia/reperfusion injury in rats

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dc.contributor.authorVELİOĞLU ÖĞÜNÇ, AYLİZ
dc.contributor.authorsSener, Goksel; Sehirli, Ozer; Velioglu-Ogunc, Ayliz; Cetinel, Sule; Gedik, Nursal; Caner, Metin; Sakarcan, Abdullah; Yegen, Berrak C.
dc.date.accessioned2022-03-10T15:25:01Z
dc.date.available2022-03-10T15:25:01Z
dc.date.issued2006
dc.description.abstractBackground: Oxygen free radicals are important components involved in the pathophysiological processes observed during ischemia/reperfusion (I/R). Objective: This study was designed to assess the possible protective effect of montelukast, a selective antagonist of cysteinyl leukotriene receptor 1 (CysLT1), on renal VR injury. Methods: Wistar albino rats were unilaterally nephrectomized and subjected to 45 min of renal pedicle occlusion followed by 6 h of reperfusion. Montelukast (10 mg kg(-1), i.p.) or saline was administered at 15 min prior to ischemia and immediately before the reperfusion period. At the end of the reperfusion period, following decapitation, kidney samples were taken for histological examination or for determination of renal malondialdehyde (MDA), an end product of lipid peroxidation; glutathione (GSH), a key antioxidant; and myeloperoxidase (MPO) activity, an index of tissue neutrophil infiltration. Formation of reactive oxygen species in renal tissue samples was monitored by using chemiluminescence (CL) technique with luminol and lucigenin probes. Creatinine, blood urea nitrogen and lactate dehydrogenase (LDH) activity were measured in the serum samples, while leukotriene B-4, TNF-alpha, IL-beta, JL-6 and total antioxidant capacity (AOC) were assayed in plasma samples. Results: Ischemia/reperfusion caused a significant decrease in renal GSH and plasma AOC, which was accompanied with significant increases in MDA level, MPO activity, and CL levels of the renal tissue concomitant with increased levels of the pro-inflammatory mediators, LDH activity, creatinine and BUN. On the other hand, montelukast treatment reversed all these biochemical indices as well as histopathological alterations induced by I/R. Conclusions: CysLT I receptor antagonist montelukast reversed I/R-induced oxidant responses, improved microscopic damage and renal function. It seems likely that montelukast protects kidney tissue by inhibiting neutrophil infiltration, balancing oxidant-antioxidant status, and regulating the generation of inflammatory mediators. (c) 2006 Elsevier Ltd. All rights reserved.
dc.identifier.doi10.1016/j.phrs.2006.02.007
dc.identifier.issn1043-6618
dc.identifier.pubmed16584888
dc.identifier.urihttps://hdl.handle.net/11424/220059
dc.identifier.wosWOS:000238867000011
dc.language.isoeng
dc.publisherACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
dc.relation.ispartofPHARMACOLOGICAL RESEARCH
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectleukotrienes
dc.subjectmontelukast
dc.subjectischemia/reperfusion
dc.subjectkidney
dc.subjectmyeloperoxidase
dc.subjectcytokines
dc.subjectISCHEMIA-REPERFUSION INJURY
dc.subjectSUPERIOR MESENTERIC-ARTERY
dc.subjectBLT RECEPTOR ANTAGONIST
dc.subjectLEUKOTRIENES
dc.subjectDYSFUNCTION
dc.subjectETHANOL
dc.subjectSEPSIS
dc.subjectMICE
dc.titleMontelukast protects against renal ischemia/reperfusion injury in rats
dc.typereview
dspace.entity.typePublication
local.avesis.idf3562d15-18ef-4607-bf60-75e45d2f42ff
local.import.packageSS5
local.indexed.atWOS
local.indexed.atSCOPUS
local.indexed.atPUBMED
local.journal.numberofpages7
oaire.citation.endPage71
oaire.citation.issue1
oaire.citation.startPage65
oaire.citation.titlePHARMACOLOGICAL RESEARCH
oaire.citation.volume54
relation.isAuthorOfPublication13300bf6-ba96-4f87-9868-b0d2c86f572a
relation.isAuthorOfPublication.latestForDiscovery13300bf6-ba96-4f87-9868-b0d2c86f572a

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