IL-5 blocks apoptosis and tau hyperphosphorylation induced by Abeta25-35 peptide in PC12 cells
J. physiol. biochem
; 73(2): 259-266, mayo 2017. graf
Artigo
em Inglês
| IBECS
| ID: ibc-168482
Biblioteca responsável:
ES1.1
Localização: BNCS
ABSTRACT
The primary features of Alzheimers disease (AD) are extracellular amyloid plaques consisting mainly of deposits of amyloid β (Aβ) peptides and intracellular neurofibrillary tangles (NFTs). Sets of evidence suggest that interleukin-5 (IL-5) is involved in the pathogenesis of AD. Herein, we investigated the protective role of IL-5 in PC12 cells, to provide new insights into understanding this disease. Western blot was employed to assess the protein levels of Bax and phospho-tau as well as phospho-JAK2; MTT assay was performed to decipher cell viability. Treatment of IL-5 decreased Aβ25-35-induced tau phosphorylation and apoptosis, effects blunted by JAK2 inhibition. IL-5 prevents Aβ25-35-evoked tau protein hyperphosphorylation and apoptosis through JAK2 signaling (AU)
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Bases de dados nacionais
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Espanha
Base de dados:
IBECS
Assunto principal:
Processamento de Proteína Pós-Traducional
/
Peptídeos beta-Amiloides
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Interleucina-5
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Proteínas tau
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Apoptose
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Subunidade alfa de Receptor de Interleucina-5
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Neurônios
Limite:
Animais
Idioma:
Inglês
Revista:
J. physiol. biochem
Ano de publicação:
2017
Tipo de documento:
Artigo
Instituição/País de afiliação:
Luohe Medical College/China