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Naringin Protects against Rotenone-induced Apoptosis in Human Neuroblastoma SH-SY5Y Cells
The Korean Journal of Physiology and Pharmacology ; : 281-285, 2009.
Artigo em Inglês | WPRIM | ID: wpr-727523
ABSTRACT
Rotenone, a mitochondrial complex I inhibitor, can induce the pathological features of Parkinson's disease (PD). In the present study, naringin, a grapefruit flavonoid, inhibited rotenone-induced cell death in human neuroblastoma SH-SY5Y cells. We assessed cell death and apoptosis by measuring mitogen-activated protein kinase (MAPKs) and caspase (CASPs) activities and by performing 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, 4,6-diamidino-2-phenylindole (DAPI) staining, and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining. Naringin also blocked rotenone-induced phosphorylation of Jun NH2-terminal protein kinase (JNK) and P38, and prevented changes in B-cell CLL/lymphoma 2 (BCL2) and BCL2-associated X protein (BAX) expression levels. In addition, naringin reduced the enzyme activity of caspase 3 and cleavages of caspase 9, poly (ADP-ribose) polymerase (PARP), and caspase 3. These results suggest that naringin has a neuroprotective effect on rotenone-induced cell death in human neuroblastoma SH-SY5Y cells.
Assuntos

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Doença de Parkinson / Fosforilação / Proteínas Quinases / Rotenona / Sais de Tetrazólio / Tiazóis / Linfócitos B / Morte Celular / Apoptose / Fármacos Neuroprotetores Limite: Humanos Idioma: Inglês Revista: The Korean Journal of Physiology and Pharmacology Ano de publicação: 2009 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Doença de Parkinson / Fosforilação / Proteínas Quinases / Rotenona / Sais de Tetrazólio / Tiazóis / Linfócitos B / Morte Celular / Apoptose / Fármacos Neuroprotetores Limite: Humanos Idioma: Inglês Revista: The Korean Journal of Physiology and Pharmacology Ano de publicação: 2009 Tipo de documento: Artigo