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Provedor de dados:  BJMBR
País:  Brazil
Título:  Protection against neurotoxicity by an autophagic mechanism
Autores:  Liu,Kangyong
Huang,Jiankang
Chen,Rongfu
Zhang,Ting
Shen,Liwei
Yang,Jiajun
Sun,Xiaojiang
Data:  2012-05-01
Ano:  2012
Palavras-chave:  3-N-butylphthalide
Parkinson’s disease
Α-synuclein
PC12 cells
Autophagy
Resumo:  The objective of the present study was to investigate the effects of 3-n-butylphthalide (NBP) on a 1-methyl-4-phenylpyridinium (MPP+)-induced cellular model of Parkinson’s disease (PD) and to illustrate the potential mechanism of autophagy in this process. For this purpose, rat PC12 pheochromocytoma cells were treated with MPP+ (1 mM) for 24 h following pretreatment with NBP (0.1 mM). Cell metabolic viability was determined by the MTT assay and cell ultrastructure was examined by transmission electron microscopy. The intracellular distribution and expression of α-synuclein and microtubule-associated protein light chain 3 (LC3) were detected by immunocytochemistry and Western blotting. Our results demonstrated that: 1) NBP prevented MPP+-induced cytotoxicity in PC12 cells by promoting metabolic viability. 2) NBP induced the accumulation of autophagosomes in MPP+-treated PC12 cells. 3) Further study of the molecular mechanism demonstrated that NBP enhanced the colocalization of α-synuclein and LC3 and up-regulated the protein level of LC3-II. These results demonstrate that NBP protects PC12 cells against MPP+-induced neurotoxicity by activating autophagy-mediated α-synuclein degradation, implying that it may be a potential effective therapeutic agent for the treatment of PD.
Tipo:  Info:eu-repo/semantics/article
Idioma:  Inglês
Identificador:  http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2012000500004
Editor:  Associação Brasileira de Divulgação Científica
Relação:  10.1590/S0100-879X2012007500039
Formato:  text/html
Fonte:  Brazilian Journal of Medical and Biological Research v.45 n.5 2012
Direitos:  info:eu-repo/semantics/openAccess
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