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Delayed Therapeutic Administration of Melatonin Enhances Neuronal Survival Through AKT and MAPK Signaling Pathways Following Focal Brain Ischemia in Mice

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dc.contributor.authorKilic, Ulkan
dc.contributor.authorELİBOL, BİRSEN
dc.contributor.authorÇAĞLAYAN, AHMET BURAK
dc.contributor.authorBeker, Mustafa Caglar
dc.contributor.authorBeker, Merve
dc.contributor.authorAltug-Tasa, Burcugul
dc.contributor.authorUYSAL, ÖMER
dc.contributor.authorYILMAZ, BAYRAM
dc.contributor.authorKILIÇ, ERTUĞRUL
dc.contributor.institutionauthorELİBOL, BİRSEN
dc.date.accessioned2022-04-05T20:59:11Z
dc.date.available2022-04-05T20:59:11Z
dc.date.issued2022-03-01T00:00:00Z
dc.description.abstractMelatonin has a role in the cell survival signaling pathways as a candidate for secondary stroke prevention. Therefore, in the present study, the coordination of ipsilateral and contralateral hemispheres to evaluate delayed post-acute effect of melatonin was examined on recovery of the cell survival and apoptosis after stroke. Melatonin was administered (4 mg/kg/day) intraperitoneally for 45 days, starting 3 days after 30 min of middle cerebral artery occlusion. The genes and proteins related to the cell survival and apoptosis were investigated by immunofluorescence, western blotting, and RT-PCR techniques after behavioral experiments. Melatonin produced delayed neurological recovery by improving motor coordination on grip strength and rotarod tests. This neurological recovery was also reflected by high level of NeuN positive cells and low level of TUNEL-positive cells suggesting enhanced neuronal survival and reduced apoptosis at the fifty-fifth day of stroke. The increase of NGF, Nrp1, c-jun; activation of AKT; and dephosphorylation of ERK and INK at the fifty-fifth day showed that cell survival and apoptosis signaling molecules compete to contribute to the remodeling of brain. Furthermore, an increase in the CREB and Atf-1 expressions suggested the melatonin-s strong reformative effect on neuronal regeneration. The contralateral hemisphere was more active at the latter stages of the molecular and functional regeneration which provides a further proof of principle about melatonin-s action on the promotion of brain plasticity and recovery after stroke.
dc.identifier.citationKilic U., ELİBOL B., ÇAĞLAYAN A. B. , Beker M. C. , Beker M., Altug-Tasa B., UYSAL Ö., YILMAZ B., KILIÇ E., -Delayed Therapeutic Administration of Melatonin Enhances Neuronal Survival Through AKT and MAPK Signaling Pathways Following Focal Brain Ischemia in Mice-, JOURNAL OF MOLECULAR NEUROSCIENCE, 2022
dc.identifier.doi10.1007/s12031-022-01995-y
dc.identifier.pubmed35307786
dc.identifier.scopus85126790431
dc.identifier.urihttp://hdl.handle.net/20.500.12645/30499
dc.identifier.wosWOS:000770956000001
dc.titleDelayed Therapeutic Administration of Melatonin Enhances Neuronal Survival Through AKT and MAPK Signaling Pathways Following Focal Brain Ischemia in Mice
dc.typeArticle
dspace.entity.typePublication
local.avesis.id0614edb3-dc76-448d-b826-3abd5a99c5d0
local.publication.isinternational1
relation.isAuthorOfPublication1b1887fb-6b32-44b1-9d9f-416616dc6734
relation.isAuthorOfPublication.latestForDiscovery1b1887fb-6b32-44b1-9d9f-416616dc6734
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