ArticleInternational journal of molecular sciences2016
Auraptene and Other Prenyloxyphenylpropanoids Suppress Microglial Activation and Dopaminergic Neuronal Cell Death in a Lipopolysaccharide-Induced Model of Parkinson's Disease.
Article in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- Mitochondrial quality control in neurodegenerative diseases: from molecular mechanisms to natural product therapies.Frontiers in physiology · 2025Pooled it
- C18:0 GM3 ganglioside's efficacy in LPS-induced parkinsonism: neuroprotection, inflammatory inhibition and gliosis mitigation.Behavioral and brain functions : BBF · 2025Article
- Loss of microglial Arid1a exacerbates microglial scar formation via elevated CCL5 after traumatic brain injury.Cell communication and signaling : CCS · 2024Article
- Quassinoids from Twigs ofInternational journal of molecular sciences · 2023Article
- Effects ofAntioxidants (Basel, Switzerland) · 2023Article
- Protection of Mitochondrial Potential and Activity by Oxyprenylated Phenylpropanoids.Antioxidants (Basel, Switzerland) · 2023Article
- A Narrative Review of the Effects of Citrus Peels and Extracts on Human Brain Health and Metabolism.Nutrients · 2022Review
- Article
- 7-Isopentenyloxycoumarin: What Is New across the Last Decade.Molecules (Basel, Switzerland) · 2020Review
- Citrus Auraptene Induces Expression of Brain-Derived Neurotrophic Factor in Neuro2a Cells.Molecules (Basel, Switzerland) · 2020Article
- Novel nano-vehicle for delivery and efficiency of anticancer auraptene against colon cancer cells.Scientific reports · 2020Article
- Potency of Selected Berries, Grapes, and Citrus Fruit as Neuroprotective Agents.Evidence-based complementary and alternative medicine : eCAM · 2020Review
- Citrus Auraptene Induces Glial Cell Line-Derived Neurotrophic Factor in C6 Cells.International journal of molecular sciences · 2019Article
- Auraptene Mitigates Parkinson's Disease-Like Behavior by Protecting Inhibition of Mitochondrial Respiration and Scavenging Reactive Oxygen Species.International journal of molecular sciences · 2019Article
- Auraptene-induced cytotoxicity mechanisms in human malignant glioblastoma (U87) cells: role of reactive oxygen species (ROS).EXCLI journal · 2019Article
- Inhibitory Effects of Auraptene and Naringin on Astroglial Activation, Tau Hyperphosphorylation, and Suppression of Neurogenesis in the Hippocampus of Streptozotocin-Induced Hyperglycemic Mice.Antioxidants (Basel, Switzerland) · 2018Article
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In patients with Parkinson's disease (PD), hyperactivated inflammation in the brain, particularly microglial hyperactivation in the substantia nigra (SN), is reported to be one of the triggers for the delayed loss of dopaminergic neurons and sequential motor functional impairments. We previously reported that (1) auraptene (AUR), a natural prenyloxycoumain, suppressed inflammatory responses including the hyperactivation of microglia in the ischemic brain and inflamed brain, thereby inhibiting neuronal cell death; (2) 7-isopentenyloxycoumarin (7-IP), another natural prenyloxycoumain, exerted anti-inflammatory and neuroprotective effects against excitotoxicity; and (3) 4'-geranyloxyferulic acid (GOFA), a natural prenyloxycinnamic acid, also exerted anti-inflammatory effects. In the present study, using an intranigral lipopolysaccharide (LPS)-induced PD-like mouse model, we investigated whether AUR, 7-IP, and GOFA suppress microglial activation and protect against dopaminergic neuronal cell death in the SN. We successfully showed that these prenyloxyphenylpropanoids exhibited these prospective abilities, suggesting the potential of these compounds as neuroprotective agents for patients with PD.
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Registered trials
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