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Oxidative renal damage in pyelonephritic rats is ameliorated by montelukast, a selective leukotriene CysLT1 receptor antagonist

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dc.contributor.authorVELİOĞLU ÖĞÜNÇ, AYLİZ
dc.contributor.authorsTugtepe, Halil; Sener, Goksel; Cetinel, Sule; Velioglu-Ogunc, Ayliz; Yegen, Berrak C.
dc.date.accessioned2022-03-12T17:32:24Z
dc.date.available2022-03-12T17:32:24Z
dc.date.issued2007
dc.description.abstractUrinary tract infections may induce severe inflammation, transient impairment in renal function and scar formation, ranging in severity from acute symptomatic pyelonephritis to chronic pyelonephritis, which have a potential to lead to renal failure and death. The present study aimed to investigate the possible protective effect of montelukast, a selective antagonist of cysteinyl leukotriene receptor I (leukotriene CysLT1), against Escherichia coli-induced oxidative injury and scarring in renal tissue. Wistar rats were injected 0.1 ml of E. coli (ATCC 25922 10(10) cfu/ml) or saline into left renal medullae. Six rats were assigned as the sham group and were given 0.1 ml 0.9% NaCl. Pyelonephritic rats were treated with either saline or montelukast immediately after surgery and at daily intervals. Twenty-four hours or one week after E. coli injection, rats were decapitated and the kidney samples were taken for histological examination or determination of renal malondialdehyde, glutathione (GSH) levels, myeloperoxidase (MPO) activity, and collagen contents. Formation of reactive oxygen species in renal tissue samples was monitored by using chemiluminescence technique with luminol and lucigenin probes. Creatinine, blood urea nitrogen and lactate dehydrogenase (LDH) activity were measured in the serum samples. E. coli inoculation caused significant increases in malondialdehyde level, MPO activity, chemiluminescence levels and collagen content, while GSH level was decreased in the renal tissues (p < 0.05-0.001). On the other hand, serum TNF-alpha, LDH, blood urea nitrogen and serum creatinine levels were elevated in the pyelonephritic rats as compared to control group. Leukotriene CysLT1 receptor antagonist montelukast reversed all these biochemical indices, as well as histopathological alterations, that were induced by acute pyelonephritis. It seems likely that montelukast protects kidney tissue by inhibiting neutrophil infiltration, balancing oxidant-antioxidant status, and regulating the generation of inflammatory mediators suggesting a future role for leukotriene CysLT1 receptor antagonists in the treatment of pyclonephritis. (c) 2006 Elsevier B.V. All rights reserved.
dc.identifier.doi10.1016/j.ejphar.2006.11.009
dc.identifier.eissn1879-0712
dc.identifier.issn0014-2999
dc.identifier.pubmed17173892
dc.identifier.urihttps://hdl.handle.net/11424/228564
dc.identifier.wosWOS:000244124300011
dc.language.isoeng
dc.publisherELSEVIER SCIENCE BV
dc.relation.ispartofEUROPEAN JOURNAL OF PHARMACOLOGY
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectEscherichia coli
dc.subjectmontelukast
dc.subjectglutathione
dc.subjectlipid peroxidation
dc.subjectmyeloperoxidase activity
dc.subjectTNF-alpha
dc.subjectESCHERICHIA-COLI PYELONEPHRITIS
dc.subjectHEMODIALYSIS-PATIENTS
dc.subjectBLOCKER MONTELUKAST
dc.subjectREPERFUSION INJURY
dc.subjectACUTE SUPPURATION
dc.subjectIN-VIVO
dc.subjectGLOMERULONEPHRITIS
dc.subjectSUPPRESSION
dc.subjectMECHANISMS
dc.subjectINHIBITION
dc.titleOxidative renal damage in pyelonephritic rats is ameliorated by montelukast, a selective leukotriene CysLT1 receptor antagonist
dc.typearticle
dspace.entity.typePublication
local.avesis.idf0eb06b4-0732-4295-bdee-3bd0151beddf
local.import.packageSS17
local.indexed.atWOS
local.indexed.atSCOPUS
local.indexed.atPUBMED
local.journal.numberofpages7
oaire.citation.endPage75
oaire.citation.issue1
oaire.citation.startPage69
oaire.citation.titleEUROPEAN JOURNAL OF PHARMACOLOGY
oaire.citation.volume557
relation.isAuthorOfPublication13300bf6-ba96-4f87-9868-b0d2c86f572a
relation.isAuthorOfPublication.latestForDiscovery13300bf6-ba96-4f87-9868-b0d2c86f572a

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