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Study on norcantharidin-induced apoptosis in SMMC-7721 cells through mitochondrial pathways / 中国结合医学杂志
Chinese journal of integrative medicine ; (12): 448-452, 2010.
Artigo em Inglês | WPRIM | ID: wpr-308738
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the mechanism of norcantharidin (NCTD)-induced SMMC-7721 hepatoma cell apoptosis.</p><p><b>METHODS</b>SMMC-7721 cell growth inhibition was measured by the MTT method. Apoptosis was detected by Annexin V/propidium iodide staining. The mitochondrial membrane potential was measured by flow cytometry. Western blot analysis was used to evaluate the level of cytochrome c, caspase-3, AIF, Bcl-2 and Bax expression.</p><p><b>RESULTS</b>NCTD inhibited SMMC-7721 cell growth in a time- and dose-dependent manner. The cells treated with NCTD showed the loss of mitochondrial membrane potential. The activities of caspase-3, cytochrome c, AIF, and Bax were up-regulated after NCTD treatment at different doses. The expression of Bcl-2 was decreased after treatment with NCTD.</p><p><b>CONCLUSIONS</b>NCTD could induce SMMC-7721 cell apoptosis. The activation of the mitochondrial pathway was involved in the process of NCTD-induced SMMC-7721 cell apoptosis.</p>
Assuntos
Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Patologia / Farmacologia / Western Blotting / Apoptose / Compostos Bicíclicos Heterocíclicos com Pontes / Linhagem Celular Tumoral / Citocromos c / Fator de Indução de Apoptose / Proteína X Associada a bcl-2 / Caspase 3 Limite: Humanos Idioma: Inglês Revista: Chinese journal of integrative medicine Ano de publicação: 2010 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Patologia / Farmacologia / Western Blotting / Apoptose / Compostos Bicíclicos Heterocíclicos com Pontes / Linhagem Celular Tumoral / Citocromos c / Fator de Indução de Apoptose / Proteína X Associada a bcl-2 / Caspase 3 Limite: Humanos Idioma: Inglês Revista: Chinese journal of integrative medicine Ano de publicação: 2010 Tipo de documento: Artigo