Soluble Epoxide Hydrolase Deficiency or Inhibition Attenuates MPTP-Induced Parkinsonism

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• 作者：Xiaocui Qin ; Qiaoqi Wu ; Lifang Lin ; Aimin Sun ; Shuhu Liu…
• 关键词：Soluble epoxide hydrolase ; EET ; Parkinson’s disease ; MPTP
• 刊名：Molecular Neurobiology
• 出版年：2015
• 出版时间：August 2015
• 年：2015
• 卷：52
• 期：1
• 页码：187-195
• 全文大小：2,355 KB
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• 作者单位：Xiaocui Qin (1)
  Qiaoqi Wu (1)
  Lifang Lin (1)
  Aimin Sun (2)
  Shuhu Liu (1)
  Xiaowen Li (1)
  Xiong Cao (1)
  Tianming Gao (1)
  Pengcheng Luo (3)
  Xinhong Zhu (1)
  Xuemin Wang (1)
  
  1. Department of Neurobiology, Southern Medical University, Guangzhou, Guangdong Province, China
  2. Department of Radiology, Southern Medical University, Guangzhou, Guangdong Province, China
  3. Huangshi Central Hospital, Hubei Polytechnic University, Hubei Province, China
  
• 刊物主题：Neurosciences; Neurobiology; Cell Biology; Neurology;
• 出版者：Springer US
• ISSN：1559-1182

文摘

Soluble epoxide hydrolase (sEH) inhibition has been demonstrated to have beneficial effects on various diseases, such as hypertension, diabetes, and brain ischemia. However, whether sEH inhibition has therapeutic potential in Parkinson’s disease is still unknown. In this paper, we found that sEH expression is increased in 1-methyl-4-phenyl-1,2,3,6-tetrahydro pyridine (MPTP)-treated mice, and sEH deficiency and inhibition significantly attenuated tyrosine hydroxylase (TH)-positive cell loss and improved rotarod performance. The substrate of sEH, 14,15-epoxyeicosatrienoic acid (14,15-EET), protected TH-positive cells and alleviated the rotarod performance deficits of wild-type mice but not sEH-knockout mice. Moreover, the 14,15-EET antagonist 14,15-epoxyeicosa-5(Z)-enoic acid (14,15-EEZE) abolished the neuronal protective effects of sEH deficiency. In primary cultured cortical neurons, MPP+ induced significant Akt inactivation in neurons from sEH wild-type mice, and this effect was not observed in neurons from knockout mice. Our data indicate that sEH deficiency and inhibition increased 14,15-EET in MPTP-treated mice, which activated the Akt-mediated protection of TH-positive neurons and behavioral functioning. We also found that sEH deficiency attenuated TH-positive cell loss in a paraquat-induced mouse model of Parkinson’s. Our data suggest that sEH inhibition might be a powerful tool to protect dopaminergic neurons in Parkinson’s disease.