ASIA unversity:Item 310904400/16828
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    题名: Gambogenic acid induced mitochondrial-dependent apoptosis and referred to Phospho-Erk1/2 and Phospho-p38 MAPK in Human Hepatoma HepG2 Cells
    作者: 張竣維;Hebron, C.Chang;李慶林;Li, Qinglin
    贡献者: 生物科技學系
    关键词: Gambogenic acid;HepG2;Apoptosis;Mitochondrial oxidative stress;Phospho-Erk1/2 MAPK;Phospho-p38 MAPK
    日期: 2012-03
    上传时间: 2012-11-23 17:17:28 (UTC+8)
    摘要: Gambogenic acid, identified from Gamboge, is responsible for anti-tumor effects, and has been shown to be a potential molecule against human cancers. In this study, the molecular mechanism of gambogenic acid-induced apoptosis in HepG2 cells was investigated. Gambogenic acid significantly inhibited cell proliferation and induced apoptosis. Acridine orange/ethidium bromide (AO/EB) staining was used to observe apoptosis, and then confirmed by transmission electron microscopy. Gambogenic acid induced apoptosis and morphological changes in mitochondria, and intracellular reactive oxygen species (ROS) and mitochondrial membrane permeabilization (MMP) in mitochondrial apoptosis pathway were also examined. Results showed that the levels of Phospho-p38 and its downstream Phospho-Erk1/2 of HepG2 cells increased in time- and concentration-dependent manners after gambogenic acid treatments. Additionally, gambogenic acid increased expression ratio of Bcl-2/Bax in mRNA levels, Western blotting analysis also further confirmed the reduced level of Bcl-2 and increase the expression level of Bax in HepG2 cells. These results indicated that gambogenic acid induced mitochondrial oxidative stress and activated caspases through a caspase-3 and caspase-9-dependent apoptosis pathway. Moreover, gambogenic acid mediated apoptosis and was involved in the Phospho-Erk1/2 and Phospho-p38 MAPK proteins expression changes in HepG2 cells.
    關聯: ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY, V.33 N.2 :181–190.
    显示于类别:[生物科技學系] 期刊論文

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