Data/hora: 05/06/2024 04:23:48

Provedor de dados: 	56	
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	
Fonte: 	info:eu-repo/semantics/openAccess