ASIA unversity:Item 310904400/8288
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    题名: Baicalein-Induced Apoptosis via Endoplasmic Reticulum Stress Through Elevations of Reactive Oxygen Species and Mitochondria Dependent Pathway in Mouse-Rat Hybrid Retina Ganglion Cells (N18)
    作者: Li, YC (Li, Yu-Ching);Lin, HJ (Lin, Hui-Ju);Yang, JH (Yang, Jen-Hung);Yang, JS (Yang, Jai-Sing);Ho, HC (Ho, Heng-Chien);Chang, SJ (Chang, Shu-Jen);Hsai, TC (Hsai, Te-Chun);Lu, HF (Lu, Hsu-Feng);Huang, AC (Huang, An-Cheng);Chung, JG (Chung, Jing-Gung)
    贡献者: Department of Biotechnology
    关键词: Baicalein;Reactive oxygen species (ROS);Cytochrome c;Cytoplasmic Ca2+;Caspase-3;Mitochondrial death pathway;1,2-Bis(2-aminophenoxy) ethane-N,N,N ',N '-tetraacetic acid (BAPTA);Apoptosis
    日期: 2009-03
    上传时间: 2010-03-26 02:29:35 (UTC+0)
    出版者: Asia University
    摘要: Studies were designed to investigate the effects of baicalein on mouse-rat hybrid retina ganglion cells (N18) to better understand its effect on apoptosis and apoptosis-related genes in vitro. Cell viability, reactive oxygen species (ROS), cytoplasmic Ca2+, mitochondrial membrane potential (MMP), apoptosis induction, and caspases-3 activity were examined by flow cytometric assay. Apoptosis-associated proteins such as p53, Bax, Bcl-2, cytochrome c, and caspase-3 were examined by Western blot. We demonstrated the increase in the levels of p53, Bax, and cytochrome c and decrease in the level of Bcl-2, which are associated with the induction of apoptotic cell death after 24 h treatment with baicalein in N18 cells. Baicalein induced an increase in the cytoplasmic levels of ROS and Ca2+ in 1 h and reached their peak at 3 h, and thereafter a loss of MMP by flow cytometry. We also demonstrated a release of the cytochrome c from mitochondria into cytosol and an activation of caspase-3, which led to the occurrence of apoptosis in N18 cells treated with baicalein by Western blot. Pretreatment was conducted with BAPTA (intracellular calcium chelator) in baicalein-treated cells, the decline of MMP was recovered, and the increase in the level of cytoplasmic Ca2+ was suppressed, and the proportion of apoptosis was also markedly diminished. In conclusion, our data suggests that oxidative stress and cellular Ca2+ modulates the baicalein-induced cell death via a Ca2+-dependent mitochondrial death pathway in N18 cells.
    關聯: NEUROCHEMICAL RESEARCH 34 (3): 418-429
    显示于类别:[生物科技學系] 期刊論文

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