Data/hora: 13/06/2024 00:33:47

Provedor de dados: 	56	
País: 	Brazil	
Título: 	ERKs and mitochondria-related pathways are essential for glycyrrhizic acid-mediated neuroprotection against glutamate-induced toxicity in differentiated PC12 cells	
Autores: 	Wang,D.; Guo,T.Q.; Wang,Z.Y.; Lu,J.H.; Liu,D.P.; Meng,Q.F.; Xie,J.; Zhang,X.L.; Liu,Y.; Teng,L.S.	
Data: 	2014-09-01	
Ano: 	2014	
Palavras-chave: 	Glycyrrhizic acid; Neuroprotection; Glutamate; ERKs; Mitochondria.	
Resumo: 	The present study focuses on the neuroprotective effect of glycyrrhizic acid (GA, a major compound separated from Glycyrrhiza Radix, which is a crude Chinese traditional drug) against glutamate-induced cytotoxicity in differentiated PC12 (DPC12) cells. The results showed that GA treatment improved cell viability and ameliorated abnormal glutamate-induced alterations in mitochondria in DPC12 cells. GA reversed glutamate-suppressed B-cell lymphoma 2 levels, inhibited glutamate-enhanced expressions of Bax and cleaved caspase 3, and reduced cytochrome C (Cyto C) release. Exposure to glutamate strongly inhibited phosphorylation of AKT (protein kinase B) and extracellular signal-regulated kinases (ERKs); however, GA pretreatment enhanced activation of ERKs but not AKT. The presence of PD98059 (a mitogen-activated protein/extracellular signal-regulated kinase kinase [MEK] inhibitor) but not LY294002 (a phosphoinositide 3-kinase [PI3K] inhibitor) diminished the potency of GA for improving viability of glutamate-exposed DPC12 cells. These results indicated that ERKs and mitochondria-related pathways are essential for the neuroprotective effect of GA against glutamate-induced toxicity in DPC12 cells. The present study provides experimental evidence supporting GA as a potential therapeutic agent for use in the treatment of neurodegenerative diseases.	
Tipo: 	Info:eu-repo/semantics/article	
Idioma: 	Inglês	
Identificador: 	http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2014000900773	
Editor: 	Associação Brasileira de Divulgação Científica	
Relação: 	10.1590/1414-431X20143760	
Formato: 	text/html	
Fonte: 	Brazilian Journal of Medical and Biological Research  v.47 n.9 2014	
Fonte: 	info:eu-repo/semantics/openAccess