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Antiproliferative effects mechanism of beta-sitosterul in hepatoma HepG2 cells / 中国中药杂志
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-283239
Biblioteca responsável: WPRO
ABSTRACT
<p><b>OBJECTIVE</b>To study the antiproliferative effects of beta-sitosterul and its mechanism in hepatoma HepG2 cells.</p><p><b>METHOD</b>Cell proliferation was assessed by MTT assay. Cell cycle distribution, apoptosis and mitochondrial membrane potential were measured by high content screening (HCS). The protein expression of caspase-3, caspase-8, caspase-9, Bcl-2, Bax, tBid and cytochrome c in the HepG2 cells were evaluated by Western Blots.</p><p><b>RESULT</b>beta-Sitosterul exerted significant antiproliferative effects in HepG2 cells. Furthermore, beta-sitosterul also induced HepG2 cells apoptosis, lost mitochondrial membrane potential, activated caspase-3, caspase-8 and caspase-9, up-regulate Bax, tBid protein, down-regulation Bcl-2 protein. However, beta-sitosterul had hardly any effects on QSG7701 cells.</p><p><b>CONCLUSION</b>beta-Sitosterul exerted antiproliferative effects and induced HepG2 cells apoptosis via mitochondrial pathway and membrane death receptor pathway.</p>
Assuntos
Texto completo: Disponível Base de dados: WPRIM (Pacífico Ocidental) Assunto principal: Patologia / Farmacologia / Sitosteroides / Ciclo Celular / Apoptose / Carcinoma Hepatocelular / Linhagem Celular Tumoral / Proliferação de Células / Proteínas Reguladoras de Apoptose / Potencial da Membrana Mitocondrial Limite: Humanos Idioma: Chinês Revista: China Journal of Chinese Materia Medica Ano de publicação: 2011 Tipo de documento: Artigo
Texto completo: Disponível Base de dados: WPRIM (Pacífico Ocidental) Assunto principal: Patologia / Farmacologia / Sitosteroides / Ciclo Celular / Apoptose / Carcinoma Hepatocelular / Linhagem Celular Tumoral / Proliferação de Células / Proteínas Reguladoras de Apoptose / Potencial da Membrana Mitocondrial Limite: Humanos Idioma: Chinês Revista: China Journal of Chinese Materia Medica Ano de publicação: 2011 Tipo de documento: Artigo
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