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dc.contributor.authorRequejo C.
dc.contributor.authorRuiz-Ortega J.A.
dc.contributor.authorCepeda H.
dc.contributor.authorSharma A.
dc.contributor.authorSharma H.S.
dc.contributor.authorOzkizilcik A.
dc.contributor.authorTian R.
dc.contributor.authorMoessler H.
dc.contributor.authorUgedo L.
dc.contributor.authorLafuente J.V.
dc.date.accessioned2020-09-02T22:26:54Z
dc.date.available2020-09-02T22:26:54Z
dc.date.issued2018
dc.identifier10.1007/s12035-017-0741-x
dc.identifier.citation55, 1, 286-299
dc.identifier.issn08937648
dc.identifier.urihttps://hdl.handle.net/20.500.12728/5975
dc.descriptionRearing in enriched environment (EE) improves the recuperation in animal models of Parkinson’s disease (PD). Administration of TiO2-nanowired cerebrolysin (CBL) could represent an additional strategy to protect or repair the nigrostriatal system. This study aims to explore morphofunctional and biochemical changes in a preclinical stage of PD testing the synergistic efficiency of combining both strategies, housing in EE, and nanodelivery of CBL. Sprague-Dawley male rats receiving intrastriatally 6- hydroxydopamine after a short evolution time were segregated into CBL group (rats receiving nanowired CBL), EE group (rats housed in EE), CBL + EE group (rats housed in EE and receiving nanowired CBL), and control group (rats without additional treatment). Prodromic stage and treatment effects were characterized by the presence of motor symptoms (amphetamine- induced rotational behavior test). Tyrosine hydroxylase (TH) immunohistochemistry and Western blot (p-Akt/ Akt and p-ERK/ERK 1/2 as survival markers and caspase-3 as apoptotic marker) were performed in striatum and SN. A decrease in motor symptoms was shown by rats receiving CBL. EE monitoring cages revealed that rats from CBL + EE group showed more significant number of laps in the wheel than EE group. In SN, CBL + EE group also presented the highest neuronal density. Moreover, p-Akt/Akt and p-ERK/ERK 1/2 ratio was significant higher and caspase-3 expression was lower in CBL + EE group. In conclusion, the combination of CBL and EE provided evidence of neuoprotectiveneurorestorative mechanisms by which this combined strategy promoted morphofunctional improvement by activation of survival pathways after dopamine depletion in a preclinical model of PD. © Springer Science+Business Media, LLC 2017.
dc.language.isoen
dc.publisherHumana Press Inc.
dc.subject6-OHDA
dc.subjectEnriched environment
dc.subjectNanowired cerebrolysin
dc.subjectNeuroprotection
dc.subjectParkinson’s disease
dc.subjectPreclinical stage
dc.subjectcaspase 3
dc.subjectcerebrolysin
dc.subjectmitogen activated protein kinase
dc.subjectmitogen activated protein kinase 1
dc.subjectmitogen activated protein kinase 3
dc.subjectnanowire
dc.subjectprotein kinase B
dc.subjecttyrosine 3 monooxygenase
dc.subjectamino acid
dc.subjectcerebrolysin
dc.subjectnanoparticle
dc.subjectneuroprotective agent
dc.subjectAkt signaling
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectcaudate nucleus
dc.subjectcontrolled study
dc.subjectcorpus striatum
dc.subjectdrug effect
dc.subjectenvironmental enrichment
dc.subjectmale
dc.subjectMAPK signaling
dc.subjectmotor dysfunction
dc.subjectnerve cell network
dc.subjectneuroprotection
dc.subjectnonhuman
dc.subjectParkinson disease
dc.subjectprotein expression
dc.subjectputamen
dc.subjectrat
dc.subjectrearing
dc.subjectsubstantia nigra
dc.subjecttherapy effect
dc.subjectanimal
dc.subjectdisease model
dc.subjectdrug delivery system
dc.subjectenvironment
dc.subjectmetabolism
dc.subjectparkinsonism
dc.subjectpathology
dc.subjectprocedures
dc.subjectSprague Dawley rat
dc.subjectAmino Acids
dc.subjectAnimals
dc.subjectDisease Models, Animal
dc.subjectDrug Delivery Systems
dc.subjectEnvironment
dc.subjectMale
dc.subjectNanoparticles
dc.subjectNeuroprotective Agents
dc.subjectParkinsonian Disorders
dc.subjectRats
dc.subjectRats, Sprague-Dawley
dc.titleNanodelivery of cerebrolysin and rearing in enriched environment induce neuroprotective effects in a preclinical rat model of Parkinson’s disease
dc.typeArticle


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