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Effect of COX-2 inhibitor meloxicam against traumatic brain injury-induced biochemical, histopathological changes and blood-brain barrier permeability

dc.contributor.authorOZEVREN, Huseyin
dc.contributor.authorSolakoglu, Seyhun
dc.contributor.authorBIBER, Necat
dc.contributor.authorDEMIRTURK, Pelin
dc.contributor.authorAKER, Fugen V.
dc.contributor.authorHAKAN, Tayfun
dc.contributor.authorToklu, Hale Z.
dc.date.accessioned2021-03-03T19:02:55Z
dc.date.available2021-03-03T19:02:55Z
dc.date.issued2010
dc.identifier.citationHAKAN T., Toklu H. Z. , BIBER N., OZEVREN H., Solakoglu S., DEMIRTURK P., AKER F. V. , "Effect of COX-2 inhibitor meloxicam against traumatic brain injury-induced biochemical, histopathological changes and blood-brain barrier permeability", NEUROLOGICAL RESEARCH, cilt.32, sa.6, ss.629-635, 2010
dc.identifier.issn0161-6412
dc.identifier.othervv_1032021
dc.identifier.otherav_5273de4a-f15b-4b38-b9c7-37e7d8dea7c7
dc.identifier.urihttp://hdl.handle.net/20.500.12627/58527
dc.identifier.urihttps://doi.org/10.1179/016164109x12464612122731
dc.description.abstractObjective: The overproduction of reactive oxygen species and resultant damage to cellular proteins or lipids of cell membranes and DNA by free radicals are the underlying mechanisms of many neuropathologies. Cyclooxygenase-2 (COX-2) inhibitors have been suggested to be neuroprotective by reducing prostanoid and free radical synthesis, or by directing arachidonic acid metabolism through alternate pathways. This study investigated the putative neuroprotective effect of the COX-2 inhibitor, meloxicam, in a rat model of diffuse brain injury.
dc.language.isoeng
dc.subjectDahili Tıp Bilimleri
dc.subjectNöroloji
dc.subjectYaşam Bilimleri
dc.subjectTemel Bilimler
dc.subjectYaşam Bilimleri (LIFE)
dc.subjectTıp
dc.subjectSağlık Bilimleri
dc.subjectSinirbilim ve Davranış
dc.subjectNEUROSCIENCES
dc.subjectKlinik Tıp (MED)
dc.subjectKlinik Tıp
dc.subjectKLİNİK NEUROLOJİ
dc.titleEffect of COX-2 inhibitor meloxicam against traumatic brain injury-induced biochemical, histopathological changes and blood-brain barrier permeability
dc.typeMakale
dc.relation.journalNEUROLOGICAL RESEARCH
dc.contributor.departmentIstanbul Haydarpasa Numune Training & Research Hospital , ,
dc.identifier.volume32
dc.identifier.issue6
dc.identifier.startpage629
dc.identifier.endpage635
dc.contributor.firstauthorID47510


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