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Curcumin induces apoptosis through the mitochondria-mediated apoptotic pathway in HT-29 cells / 浙江大学学报(英文版)(B辑:生物医学和生物技术)
Article em En | WPRIM | ID: wpr-335395
Biblioteca responsável: WPRO
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effects of curcumin on release of cytochrome c and expressions of Bcl-2, Bax, Bad, Bcl-xL, caspase-3, poly ADP-ribose polymerase (PARP), and survivin of HT-29 cells.</p><p><b>METHODS</b>HT-29 cells were treated with curcumin (0 approximately 80 micromol/L) for 24 h. The release of cytochrome c from the mitochondria and the apoptosis-related proteins Bax, Bcl-2, Bcl-xL, Bad, caspase-3, PARP, and survivin were determined by Western blot analysis and their mRNA expressions by reverse transcriptase-polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>Curcumin significantly induced the growth inhibition and apoptosis of HT-29 cells. A decrease in expressions of Bcl-2, Bcl-xL and survivin was observed after exposure to 10 approximately 80 micromol/L curcumin, while the levels of Bax and Bad increased in the curcumin-treated cells. Curcumin also induced the release of cytochrome c, the activation of caspase-3, and the cleavage of PARP in a dose-dependent manner.</p><p><b>CONCLUSION</b>These data suggest that curcumin induced the HT-29 cell apoptosis possibly via the mitochondria-mediated pathway.</p>
Assuntos
Texto completo: 1 Base de dados: WPRIM Assunto principal: Farmacologia / Fisiologia / RNA Mensageiro / Núcleo Celular / Sobrevivência Celular / Apoptose / Células HT29 / Proteínas Proto-Oncogênicas c-bcl-2 / Secreções Corporais / Curcumina Limite: Humans Idioma: En Revista: J. Zhejiang Univ., Sci. B (Internet) Ano de publicação: 2009 Tipo de documento: Article
Texto completo: 1 Base de dados: WPRIM Assunto principal: Farmacologia / Fisiologia / RNA Mensageiro / Núcleo Celular / Sobrevivência Celular / Apoptose / Células HT29 / Proteínas Proto-Oncogênicas c-bcl-2 / Secreções Corporais / Curcumina Limite: Humans Idioma: En Revista: J. Zhejiang Univ., Sci. B (Internet) Ano de publicação: 2009 Tipo de documento: Article