Agomelatine could prevent brain and cerebellum injury against LPS-induced neuroinflammation in rats

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dc.contributor.authorSavran, Meltem Karadeniz
dc.contributor.authorAslankoç, Rahime
dc.contributor.authorÖzmen, Özlem
dc.contributor.authorErzurumlu, Yalçın
dc.contributor.authorSavas, Hasan Basri
dc.contributor.authorTemel, Esra Nurlu
dc.contributor.authorBortepe, S.
dc.date.accessioned2021-02-19T21:16:09Z
dc.date.available2021-02-19T21:16:09Z
dc.date.issued2020
dc.departmentALKÜ
dc.description.abstractSepsis, systemic hyper-inflammatory immune response, causes the increase of morbidity and mortality rates due to multi-organ diseases such as neurotoxicity. Lipopolysaccharide (LPS) induces inflammation, oxidative stress and apoptosis to cause brain damage. We aimed to evaluate the antioxidant, anti-inflammatory and antiapoptotic effects of Agomelatine (AGM) on LPS induced brain damage via NF-kB signaling. Twenty-four animals were divided into three groups as control, LPS (5 mg/kg) and LPS + AGM (20 mg/kg). Six hours after the all administrations, rats were sacrificed, brain tissues were collected for biochemical, histopathological and immunohistochemical analysis. In LPS group; total oxidant status (TOS), OSI index, Caspase-8 (Cas-8), NF-k beta levels increased and Total antioxidant status (TAS) levels decreased biochemically and Cas-8, haptoglobin and IL-10 expressions increased and sirtuin-1 (SIRT-1) levels decreased immunohistochemically. AGM treatment reversed these parameters except haptoglobin levels in hippocampus and SIRT-1 levels in cerebellum. Besides, AGM treatment blocked the phosphorylation of NF-kB biochemically and ameliorated increased the levels of hyperemia, edema and degenerative changes histopathologically. In conclusion, AGM enhanced SIRT-1 levels to negatively regulate the transcription and activation of p-NF-kB/p65 which caused to ameliorate inflammation, oxidative stress and apoptosis.
dc.identifier.doi10.1016/j.cyto.2019.154957
dc.identifier.issn1043-4666
dc.identifier.issn1096-0023
dc.identifier.pmid31869757
dc.identifier.scopusqualityQ1
dc.identifier.urihttps://doi.org/10.1016/j.cyto.2019.154957
dc.identifier.urihttps://hdl.handle.net/20.500.12868/272
dc.identifier.volume127en_US
dc.identifier.wosWOS:000515418400029
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthor0-belirlenecek
dc.language.isoen
dc.publisherAcademic Press Ltd- Elsevier Science Ltd
dc.relation.ispartofCytokine
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectAgomelatine
dc.subjectSIRT-1
dc.subjectInflammation
dc.subjectOxidative stress
dc.subjectApoptosis
dc.titleAgomelatine could prevent brain and cerebellum injury against LPS-induced neuroinflammation in rats
dc.typeArticle

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