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Doctoral Thesis
DOI
https://doi.org/10.11606/T.42.2017.tde-12072017-160810
Document
Author
Full name
Nilton Barreto dos Santos
Institute/School/College
Knowledge Area
Date of Defense
Published
São Paulo, 2017
Supervisor
Committee
Munhoz, Carolina Demarchi (President)
Camarini, Rosana
Farias, Alessandro dos Santos
Fernandes, Pedro Augusto Carlos Magno
Viel, Tânia Araújo
Title in Portuguese
Participação dos glicocorticoides na progressão e no prejuízo cognitivo da encefalomielite autoimune experimental em camundongos C57BL/6.
Keywords in Portuguese
Astrócitos
Esclerose múltipla
Glicocorticoides
Hipocampo
Memória animal
Abstract in Portuguese
A esclerose multipla (EM) é uma doença neurodegenerativa autoimune. As células da glia contribuem para o agravamento da EAE. Este trabalho objetiva mostrar a influência da dexametasona, na progressão da doença e nos défcits cognitivos da EAE. Foram utilizados camundongos C57BL/6, fêmeas, divididos em 4 grupos (CONT, DEX, EAE, EAE+DEX) imunizadas com MOG e Bordetella Pertussis, tratados com dexametasona (50mg/kg). Antes e após o aparecimento dos sintomas, os animais foram submetidos a testes comportamentais de campo aberto, labirinto em cruz elevado, contexto aversivo e reconhecimento de objetos. Os animais tratados com dexametasona (EAE+DEX) apresentaram diminuição do escore clínico em relação ao grupo EAE e apresentaram comportamento do tipo ansioso. Entretanto, o tratamento com DEX promoveu diminuição da memória de trabalho. Houve aumento marcadores inflamatórios e aumento do número de astrócitos no hipocampo do grupo EAE+DEX no 26o dia. Estes dados sugerem que a dexametasona diminui a aquisição da memória e aumenta o número e reatividade astrocitária na EAE.
Title in English
Glucocorticoid involvement in the progression and cognitive impairment of experimental autoimmune encephalomyelitis in C57BL/6 mice.
Keywords in English
Animal memory
Astrocytes
Glucocorticoids
Hippocampus
Multiple sclerosis
Abstract in English
Multiple sclerosis (MS) is an autoimmune neurodegenerative disease. The glial cells contribute to the aggravation of EAE. This work aims to show an influence of dexamethasone, the progression of the disease and the cognitive deficits of EAE. Female C57BL/6 mice were divided into 4 groups (CONT, DEX, EAE, EAE+DEX) immunized with MOG and Bordetella Pertussis, treated with dexamethasone (50mg/kg). Before and after the onset of symptoms, the animals were submitted to behavioral tests open field, the elevated plus maze, the aversive context and the object recognition test. The animals treated with dexamethasone (EAE+DEX) presented a decrease in the clinical score in relation to the EAE group and presented an anxious type behavior. However, treatment with DEX promoted a decrease in the work memory. There were increased inflammatory markers and increased number of hippocampal astrocytes from the EAE+DEX group on the 26th day. These data suggest that dexamethasone decreases memory acquisition and increases the astrocytic number and reactivity in EAE.
 
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Publishing Date
2017-07-12
 
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