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Research for axon damage of tau protein in experimental autoimmune encephalo-myelitis / 中国免疫学杂志
Chinese Journal of Immunology ; (12): 620-624, 2015.
Artigo em Chinês | WPRIM | ID: wpr-463382
ABSTRACT

Objective:

To observe dynamic change of phosphorylated tau protein and non phosphorylated tau protein in axon and explore whether GSK3 in serum were related with phosphorylated tau protein in brain of EAE mice.

Methods:

Mice were randomly divided into six groupsEAE group of acute stage,EAE group of paralytic stage,EAE group of remission stage,control group of acute stage,control group of paralytic stage,control group of remission stage,each group had twelve mice.EAE model were constructed by MOG35-55 peptides in EAE group, the saline was used in control group.The nerve function scores and incidence were observed and compared.We observed degree of brain inflammation by HE staining and measured axons which contained two kinds of tau protein by immunohistochemistry.GSK3 in serum was tested to find correlation with phosphorylated tau protein in brain by ELISA method.

Results:

Nerve function scores in EAE group were higher than control group.The degree of inflammation damage was more serious in EAE group than control group,gradually enhancing with time.Phosphorylated tau protein in brain gradually increased before mice paralyzing(P<0.01),but it decreased when symptom relieved(P<0.01).GSK3 in serum were correlated with phosphorylated tau protein in brain(r=0.9326,P<0.01),linear regression equationY=2.950+0.418X.

Conclusion:

Phosphorylated tau protein in brain are correlated with axon damage and GSK3 in serum could indirectly reflect axon damage in brain.

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Tipo de estudo: Estudo prognóstico Idioma: Chinês Revista: Chinese Journal of Immunology Ano de publicação: 2015 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Tipo de estudo: Estudo prognóstico Idioma: Chinês Revista: Chinese Journal of Immunology Ano de publicação: 2015 Tipo de documento: Artigo