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dc.contributor.authorŞALVA, EMİNE
dc.contributor.authorAhmad, Sarfraz
dc.contributor.authorALAN, SAADET
dc.contributor.authorKABASAKAL, LEVENT
dc.contributor.authorElcioglu, O. Haluk
dc.contributor.authorElcioglu, H. Kubra
dc.contributor.authorAslan, Ersin
dc.date.accessioned2021-03-04T14:30:17Z
dc.date.available2021-03-04T14:30:17Z
dc.identifier.citationElcioglu H. K. , Aslan E., Ahmad S., ALAN S., ŞALVA E., Elcioglu O. H. , KABASAKAL L., "Tocilizumab's effect on cognitive deficits induced by intracerebroventricular administration of streptozotocin in Alzheimer's model", MOLECULAR AND CELLULAR BIOCHEMISTRY, cilt.420, ss.21-28, 2016
dc.identifier.issn0300-8177
dc.identifier.othervv_1032021
dc.identifier.otherav_81f1c7a8-58f9-4f99-9759-deb7f498f025
dc.identifier.urihttp://hdl.handle.net/20.500.12627/88509
dc.identifier.urihttps://doi.org/10.1007/s11010-016-2762-6
dc.description.abstractNeuroinflammation plays pivotal roles in the pathogenesis of Alzheimer's disease (AD). IL-6 is pleiotropic cytokine which plays significant pathological role in inflammatory diseases and causes prolonged inflammation. Additionally, IL-6 activates microglia cells and enhances the accumulation of amyloid-beta peptides. Moreover, IL-6 signal transduction is mediated by membrane-bound and soluble IL-6 receptors. Tocilizumab which is a humanized anti-human IL-6 receptor (IL-6R) monoclonal antibody binds to both of these receptors and inhibits IL-6 signaling by this route. The objective was to investigate tocilizumab's potential effects in the treatment of AD. Male Sprague-Dawley rats were divided into three groups: sham (control), streptozotocin (STZ), and tocilizumab-STZ. We used a single dose of intracerebroventricular (ICV) tocilizumab, beginning 1 h prior to injection of STZ for 3 weeks. The rats in STZ and tocilizumab-STZ groups were given ICV-STZ (3 mg/kg). Behavioral parameters were evaluated on days 17-20 and the rats were sacrificed on day-21 to examine histopathological changes. STZ injection caused significant decrease in the mean escape latency in passive avoidance and also declined the performance improvement in Morris water maze tests. Tocilizumab-STZ group significantly improved learning and spatial memory functions by increasing RLT in the passive avoidance and by shortening escape latency in reaching the platform in the Morris water maze. Histopathological changes were examined using hematoxylin and eosin and immunohistochemical (IHC) stainings. IHC analysis revealed that while protein expressions of amyloid- (3.5 +/- A 0.2) and IL-6 (2.9 +/- A 0.4) showed intense immune-positivity in STZ group, amyloid- (1.3 +/- A 0.1) and IL-6 (1.5 +/- A 0.2) immunoreactivities were substantially decreased in tocilizumab treatment group. We conclude that tocilizumab treatment attenuated significantly STZ-induced cognitive impairment and histopathological changes. Further studies would be desirable to investigate clinically relevant protective effects of tocilizumab in AD.
dc.language.isoeng
dc.subjectYaşam Bilimleri
dc.subjectMoleküler Biyoloji ve Genetik
dc.subjectTemel Bilimler
dc.subjectTemel Tıp Bilimleri
dc.subjectHistoloji-Embriyoloji
dc.subjectSağlık Bilimleri
dc.subjectTıp
dc.subjectYaşam Bilimleri (LIFE)
dc.subjectMoleküler Biyoloji ve Genetik
dc.subjectHÜCRE BİYOLOJİSİ
dc.titleTocilizumab's effect on cognitive deficits induced by intracerebroventricular administration of streptozotocin in Alzheimer's model
dc.typeMakale
dc.relation.journalMOLECULAR AND CELLULAR BIOCHEMISTRY
dc.contributor.departmentMarmara Üniversitesi , ,
dc.identifier.volume420
dc.identifier.startpage21
dc.identifier.endpage28
dc.contributor.firstauthorID235024


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