2,5‐hexanedione induced apoptosis of rat bone marrow mesenchymal stem cells by reactive oxygen species
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- Liu Shuang
- Department of Occupational and Environmental Health, Dalian Medical University
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- Chen Feng
- Department of Microbiology, Dalian Medical University
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- Wang Longjuan
- Department of Microbiology, Dalian Medical University
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- Sun Wenchang
- Department of Microbiology, Dalian Medical University
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- Liu Qigui
- School of Public Health, Dalian Medical University
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- Chen Haibo
- Institute of Cancer Stem Cell, Dalian Medical University
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- Su Dan
- Department of Microbiology, Dalian Medical University
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- Jiang Yue
- Department of Microbiology, Dalian Medical University
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- Piao Fengyuan
- Department of Occupational and Environmental Health, Dalian Medical University
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- Sun Xiance
- Department of Occupational and Environmental Health, Dalian Medical University
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- Sun Wenfang
- Department of Neurology, Second Affiliated Hospital, Dalian Medical University
書誌事項
- タイトル別名
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- 2,5-hexanedione induced apoptosis of rat bone marrow mesenchymal stem cells by reactive oxygen species
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Objectives: n-Hexane, a common industrial organic solvent, causes multiple organ damage, especially neurotoxicity, which is proved to be caused by its metabolite 2,5-hexanedione (2,5-HD). We previously showed that 2,5-HD induced apoptosis of rat bone marrow mesenchymal stem cells (BMSCs). In the current study, we explored the mechanism of 2,5-HD-induced apoptosis, especially the role played by reactive oxygen species (ROS). Methods: Intracellular ROS levels after 2,5-HD treatment were measured by the dichloro-dihydro-fluorescein diacetate (DCFH-DA) method, and the antioxidant N-acetyl cysteine (NAC) was used to scavenge ROS. Apoptosis, mitochondrial membrane potential (MMP), and caspase-3 activity were measured after 2,5-HD exposure with or without NAC pretreatment. Results: In rat BMSCs, 20 mM 2,5-HD significantly increased ROS levels and apoptosis. In addition, MMP activity was decreased and caspase-3 activity was increased. With NAC pretreatment, ROS increases were prevented, cells were rescued from apoptosis, and both MMP and caspase-3 activity returned to normal levels. Western blotting analysis of malondialdehyde-modified proteins and superoxide dismutase (SOD) 1 showed that after 2,5-HD exposure, BMSCs had oxidative damage and abnormal SOD1 expression. These returned to normal when cells were pretreated with NAC in addition to 20 mM 2,5-HD. Furthermore, the expressions of NF-κB p65/RelA and phospho-NF-κB p65/RelA (Ser536) were suppressed after 2,5-HD exposure and restored by NAC pretreatment. Conclusions: 2,5-HD-induced apoptosis in rat BMSCs is potentially mediated by excessive ROS production.
収録刊行物
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- journal of Occupational Health
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journal of Occupational Health 58 (2), 170-178, 2016
公益社団法人 日本産業衛生学会
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詳細情報 詳細情報について
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- CRID
- 1390001204454679680
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- NII論文ID
- 40020804283
- 130005153235
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- NII書誌ID
- AA11090645
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- ISSN
- 13489585
- 13419145
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- NDL書誌ID
- 027254977
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- PubMed
- 27010086
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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
- Crossref
- PubMed
- CiNii Articles
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- 使用不可