NAD+ Treatment Can Prevent Rotenone-Induced Increases in DNA Damage, Bax Levels and Nuclear Translocation of Apoptosis-Inducing Factor in Differentiated PC12 Cells

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• 作者：Yunyi Hong (1)
  Hui Nie (1)
  Xunbin Wei (1)
  Shen Fu (3)
  Weihai Ying (1) (2)
  
  1. Med-X Research Institute and School of Biomedical Engineering ; Shanghai Jiao Tong University ; 1954 Huashan Road ; Shanghai ; 200030 ; People鈥檚 Republic of China
  3. Radiation Oncology Department ; Shanghai Proton and Heavy Ion Center ; Shanghai ; 201321 ; People鈥檚 Republic of China
  2. Institute of Neurology ; Ruijin Hospital ; Shanghai Jiao Tong University School of Medicine ; Shanghai ; People鈥檚 Republic of China
  
• 关键词：Apoptosis ; Apoptosis ; inducing factor ; DNA double ; strand breaks ; Mitochondrial permeability transition ; NAD+ ; Necrosis
• 刊名：Neurochemical Research
• 出版年：2015
• 出版时间：April 2015
• 年：2015
• 卷：40
• 期：4
• 页码：837-842
• 全文大小：2,186 KB
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• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Biomedicine
  Neurosciences
  Biochemistry
  Neurology
  
• 出版者：Springer Netherlands
• ISSN：1573-6903

文摘

Nicotinamide adenine dinucleotide (NAD+) plays critical roles in energy metabolism, mitochondrial functions, calcium homeostasis and immunological functions. Our previous studies have found that NAD+ administration can profoundly decrease ischemic brain injury and traumatic brain injury. Our recent study has also provided first direct evidence indicating that NAD+ treatment can decrease cellular apoptosis, while the mechanisms underlying this protective effect remain unclear. In our current study, we determined the effects of NAD+ treatment on several major factors in apoptosis and necrosis, including levels of Bax and nuclear translocation of apoptosis-inducing factor (AIF), as well as levels of DNA double-strand breaks (DSBs) and intracellular ATP in rotenone-treated differentiated PC12 cells. We found that NAD+ treatment can markedly attenuate the rotenone-induced increases in the levels of Bax and nuclear translocation of AIF in the cells. We further found that NAD+ treatment can significantly attenuate the rotenone-induced increase in the levels of DSBs and decrease in the intracellular ATP levels. Collectively, our study has suggested mechanisms underlying the preventive effects of NAD+ on apoptosis, which has highlighted the therapeutic potential of NAD+ for decreasing apoptotic changes in multiple major diseases.