ArticleMolecular neurobiology2015
Soluble Epoxide Hydrolase Deficiency or Inhibition Attenuates MPTP-Induced Parkinsonism.
Article in Molecular neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 42 citations in OpenAlex.
- The Roles of EETs in Neurological Disorders.CNS neuroscience & therapeutics · 2026Review
- The soluble epoxide hydrolase inhibitor TPPU alleviates Aβ-mediated neuroinflammatory responses in Drosophila melanogaster and cellular models of alzheimer's disease.Journal of inflammation (London, England) · 2025Article
- Interaction between α-Synuclein and Bioactive Lipids: Neurodegeneration, Disease Biomarkers and Emerging Therapies.Metabolites · 2024Review
- Aflatoxin BInternational journal of molecular sciences · 2023Article
- Inhibition of soluble epoxide hydrolase reduces paraquat neurotoxicity in rodents.Environmental toxicology and pharmacology · 2023Article
- Cytochrome P450-derived eicosanoids in brain: From basic discovery to clinical translation.Advances in pharmacology (San Diego, Calif.) · 2023Article
- Soluble Epoxide Hydrolase as a Therapeutic Target for Neuropsychiatric Disorders.International journal of molecular sciences · 2022Review
- Kurarinone alleviated Parkinson's disease via stabilization of epoxyeicosatrienoic acids in animal model.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Inhibition of sEH via stabilizing the level of EETs alleviated Alzheimer's disease through GSK3β signaling pathway.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2021Article
- Discovery of Soluble Epoxide Hydrolase Inhibitors from Chemical Synthesis and Natural Products.Journal of medicinal chemistry · 2021Review
- Review
- PET imaging of soluble epoxide hydrolase in non-human primate brain with [EJNMMI research · 2020Article
- Soluble Epoxide Hydrolase Inhibition to Face Neuroinflammation in Parkinson's Disease: A New Therapeutic Strategy.Biomolecules · 2020Review
- Cytochrome P450 derived epoxidized fatty acids as a therapeutic tool against neuroinflammatory diseases.Prostaglandins & other lipid mediators · 2020Review
- A single meal has the potential to alter brain oxylipin content.Prostaglandins, leukotrienes, and essential fatty acids · 2020Article
- Neuroprotection Against Parkinson's Disease Through the Activation of Akt/GSK3β Signaling Pathway by Tovophyllin A.Frontiers in neuroscience · 2020Article
- Targeting Mitochondrial Impairment in Parkinson's Disease: Challenges and Opportunities.Frontiers in cell and developmental biology · 2020Review
- Role of epoxy-fatty acids and epoxide hydrolases in the pathology of neuro-inflammation.Biochimie · 2019Review
- The Role of Lipids in Parkinson's Disease.Cells · 2019Review
- Humble beginnings with big goals: Small molecule soluble epoxide hydrolase inhibitors for treating CNS disorders.Progress in neurobiology · 2019Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.