Publication:
Neuroprotective Effects of Acetyl-L on Lipopolysaccharide-Induced Neuroinflammation in Mice: Involvement of Brain-Derived Neurotrophic Factor

dc.authorscopusid57190279076
dc.authorscopusid6506699286
dc.contributor.authorKazak, F.
dc.contributor.authorYarim, G.F.
dc.date.accessioned2020-06-21T13:18:16Z
dc.date.available2020-06-21T13:18:16Z
dc.date.issued2017
dc.departmentOndokuz Mayıs Üniversitesien_US
dc.department-temp[Kazak] Filiz, Department of Biochemistry, Mustafa Kemal Üniversitesi, Antakya, Turkey; [Yarim] Gül Fatma, Department of Biochemistry, Ondokuz Mayis Üniversitesi, Samsun, Turkeyen_US
dc.description.abstractNeuroinflammation is the inflammation of nervous tissue that can lead to neurodegeneration. Brain-derived neurotrophic factor (BDNF) is a neurotrophin which affects growth, function and survival of neurons, enhances the stabilization of synapses, regulates synaptic function and branching of dendrites and axons. Brain-derived neurotrophic factor is believed to be involved in the pathophysiology of central nervous system (CNS) diseases associated with neuroinflamation. The aim of this study was to investigate new protective and therapeutic effect of acetyl-L-carnitine (ALCAR) in neuroinflammation. Acetyl-L-carnitine was administered into Swiss Albino mice as 100 mg/kg/day and 300 mg/kg/day for 5 days. Neuroinflammation was induced by lipopolysaccharide (LPS). Histopathological findings associated with ALCAR administration on neuroinflammation in the brain were determined. Moreover, the effects of ALCAR on BDNF concentration in the brain tissue was evaluated. The LPS administration showed higher microglial activation in the brain of LPS, 100A + LPS and 300A + LPS groups compared to that in the control (p < 0.05). In the 100A + LPS group, microglial activation was lower and BDNF concentration was higher than in the 300A + LPS group (p > 0.05). The findings suggest that the dose of ALCAR at 100 mg/kg/day i.p. may have a beneficial effect on LPS-induced neuroinflammation in mice. As a conclusion, ALCAR may be used as an optional neuroprotective and therapeutic agent to attenuate inflammatory damage in the CNS regarding BDNF, in a dose dependent manner. © 2017 Elsevier B.V.en_US
dc.identifier.doi10.1016/j.neulet.2017.07.059
dc.identifier.endpage36en_US
dc.identifier.issn0304-3940
dc.identifier.issn1872-7972
dc.identifier.pmid28822835
dc.identifier.scopus2-s2.0-85028004118
dc.identifier.scopusqualityQ2
dc.identifier.startpage32en_US
dc.identifier.urihttps://doi.org/10.1016/j.neulet.2017.07.059
dc.identifier.volume658en_US
dc.identifier.wosWOS:000414115200006
dc.identifier.wosqualityQ4
dc.language.isoenen_US
dc.publisherElsevier Ireland Ltden_US
dc.relation.ispartofNeuroscience Lettersen_US
dc.relation.journalNeuroscience Lettersen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAcetyl-L-Carnitineen_US
dc.subjectBrain-Derived Neurotrophic Factoren_US
dc.subjectLipopolysaccharideen_US
dc.subjectNeuroinflammationen_US
dc.titleNeuroprotective Effects of Acetyl-L on Lipopolysaccharide-Induced Neuroinflammation in Mice: Involvement of Brain-Derived Neurotrophic Factoren_US
dc.typeArticleen_US
dspace.entity.typePublication

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