Induction of DJ-1 protects neuronal cells from isoflurane induced neurotoxicity

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• 作者：Wenjie Liu ; Qulian Guo ; Xiaoling Hu ; Liangyu Peng ; Bin Zhou
• 关键词：Anesthetic ; Isoflurane ; DJ ; 1 ; Mitochondria ; Oxidative stress ; Apoptosis
• 刊名：Metabolic Brain Disease
• 出版年：2015
• 出版时间：June 2015
• 年：2015
• 卷：30
• 期：3
• 页码：703-709
• 全文大小：667 KB
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• 作者单位：Wenjie Liu (1) (2)
  Qulian Guo (1)
  Xiaoling Hu (2)
  Liangyu Peng (2)
  Bin Zhou (2)
  
  1. Department of Anesthesiology, Xiangya Hospital, Central South University, 87 Xiangya Road, 410008, Changsha, Hunan, China
  2. Department of Anesthesiology, The First affiliated Hospital of University of South China, Hengyang, 421001, China
  
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Biomedicine
  Neurosciences
  Neurology
  Biochemistry
  Oncology
  
• 出版者：Springer Netherlands
• ISSN：1573-7365

文摘

Oxidative stress, mitochondrial dysfunction and neuronal apoptosis are thought to be major contributors of Isoflurane toxicity. However, the underlying mechanisms remain largely to be determined. DJ-1, a protein that is involved in the response to various kinds of stress, has shown its neuroprotective effects. Whether DJ-1 has a neuroprotective effect against isoflurane-induced neurotoxocity is still unknown. In this study, we found that expression of DJ-1 is elevated in response to isoflurane treatment in human SH-SY5Y neuroblastoma cells. In order to clarify whether DJ-1 plays a potential role in isoflurane neurotoxicity or as a compensatory response for survival, we investigated the effects of DJ-1 silencing in isoflurane neurotoxicity. Our findings indicate that knockdown of DJ-1 promotes isoflurane-induced oxidative stress and mitochondrial dysfunction. Importantly, DJ-1 silencing was found to exacerbate isoflurane- induced apoptosis through modulation of mitochondria-dependent apoptosis pathways, thereby suggesting that induction of DJ-1 in response to isoflurane might act as a compensatory response for cell survival.