The Protective Effect of Silibinin Against Mitomycin C-Induced Intrinsic Apoptosis in Human Melanoma A375-S2 Cells
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- Jiang Yuan-yuan
- China-Japan Research Institute of Medical and Pharmaceutical Sciences, Shenyang Pharmaceutical University, China
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- Wang Hong-jun
- China-Japan Research Institute of Medical and Pharmaceutical Sciences, Shenyang Pharmaceutical University, China
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- Wang Jing
- China-Japan Research Institute of Medical and Pharmaceutical Sciences, Shenyang Pharmaceutical University, China
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- Tashiro Shin-ichi
- Department of Clinical and Biomedical Sciences, Showa Pharmaceutical University, Japan
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- Onodera Satoshi
- Department of Clinical and Biomedical Sciences, Showa Pharmaceutical University, Japan
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- Ikejima Takashi
- China-Japan Research Institute of Medical and Pharmaceutical Sciences, Shenyang Pharmaceutical University, China
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抄録
Silibinin is known for its hepatoprotective, anti-inflammatory, and anti-carcinogenic effects. We found that silibinin exhibited a protective effect against chemotherapeutic reagent mitomycin C–induced cell death in A375-S2 cells in a p53-dependent manner, which contradicted the findings of previous studies investigating the anti-neoplastic activity of silibinin and developing silibinin as a potential anti-neoplastic drug in clinical therapy. Mitomycin C administration triggered a time- and dose-dependent cell death in A375-S2 cells. Apoptotic morphology, DNA fragmentation, and caspase-3 activation demonstrated that the major cause of A375-S2 cell death by mitomycin C was apoptosis. This was associated with a marked increase of p53 level and changes in mitochondria associated proteins. However, preincubation with silibinin prior to mitomycin C treatment substantially suppressed cell apoptosis, attenuated the change of p53 and Bcl-2 expressions, blocked the translocation of Bax to mitochondrial outer membrane, and ameliorated the loss of mitochondrial membrane potential, but mitomycin C stimuli led to few changes in the protein levels of caspase 8, Fas ligand, and Fas-associated death domain protein, indicating that silibinin protected cells from mitomycin C–induced apoptosis mainly via suppressing the mitochondria-mediated intrinsic apoptosis pathway, but not in an extrinsic manner.<br>
収録刊行物
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- Journal of Pharmacological Sciences
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Journal of Pharmacological Sciences 111 (2), 137-146, 2009
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390282680155900672
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- NII論文ID
- 10025738980
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- NII書誌ID
- AA11806667
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- ISSN
- 13478648
- 13478613
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- NDL書誌ID
- 10403817
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
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