Mimosine-Induced Apoptosis in C6 Glioma Cells Requires the Release of Mitochondria-Derived Reactive Oxygen Species and p38, JNK Activation |
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| Authors: | Shanlou Qiao Keiko Murakami Qinghong Zhao Baoling Wang Hisao Seo Hitoshi Yamashita Xiaotao Li Takashi Iwamoto Masatoshi Ichihara Masataka Yoshino |
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| Institution: | (1) Department of Biomedical Sciences, College of Life and Health Sciences, Chubu University, Aichi 487-8501, Japan;(2) Department of Biochemistry, Aichi Medical University School of Medicine, Nagakute, Aichi 480-1195, Japan;(3) Department of Surgery, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, 210011, China;(4) Institute of Biomedical Sciences, East China Normal University, 500 Dongchuan Road, Shanghai, 200241, China;(5) Department of Food and Nutritional Environment, Kinjo Gakuin University, Omori 2-1723, Moriyama-ku, Nagoya 463-8521, Japan |
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| Abstract: | Growth-inhibitory effects of mimosine, a plant amino acid, on rat C6 glioma cells were analyzed. Mimosine markedly inhibited
proliferation and induced apoptosis of C6 glioma cells in a dose- and time-dependent manner. Mimosine-mediated apoptosis was
accompanied by promoting reactive oxygen species (ROS) generation in mitochondria, and by decreased mitochondrial membrane
potential (Δψ), and release of cytochrome c from mitochondria, followed by caspase 3 activation. Furthermore, mimosine increased the phosphorylation level of c-Jun-N-terminal
protein kinase and p38, which was the downstream effect of ROS accumulation. Mimosine was confirmed to show profound effects
on apoptosis of C6 glioma cells by ROS-regulated mitochondria pathway, and these results bear on the hypothesized potential
for mimosine as promising agents in the treatment of malignant gliomas. |
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