ArticleInternational journal of molecular sciences2018
Inhibition of Microglia-Derived Oxidative Stress by Ciliary Neurotrophic Factor Protects Dopamine Neurons In Vivo from MPP⁺ Neurotoxicity.
Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
- HSN G1 demonstrates multifaceted therapeutic strategy against Alzheimer disease in APP PS1 mouse model.Scientific reports · 2026Article
- Transient Receptor Potential Channels as Key Regulators of Neuroinflammation in Neurological Disorders: Mechanistic Insights, Therapeutic Potentials, and Future Directions.CNS neuroscience & therapeutics · 2025Review
- Association of TRPV1 and the SIRT3/SOD2 Signaling Pathway in Mononuclear Cells and Astrocyte-Derived Extracellular Vesicles in Patients with Schizophrenia.Brain sciences · 2025Article
- The possible effects of chili peppers on ADHD in relation to the gut microbiota.Frontiers in nutrition · 2025Review
- Effects of a ciliary neurotrophic factor (CNTF) small-molecule peptide mimetic in an in vitro and in vivo model of CDKL5 deficiency disorder.Journal of neurodevelopmental disorders · 2024Article
- Research trends and hotspots of ferroptosis in neurodegenerative diseases from 2013 to 2023: A bibliometrics study.Heliyon · 2024Article
- Oxidative Stress and Dopaminergic Metabolism: A Major PD Pathogenic Mechanism and Basis of Potential Antioxidant Therapies.CNS & neurological disorders drug targets · 2024Review
- Therapeutic Potential of Capsaicin in Various Neurodegenerative Diseases with Special Focus on Nrf2 Signaling.Current pharmaceutical biotechnology · 2024Review
- Impact of TRPV1 on Pathogenesis and Therapy of Neurodegenerative Diseases.Molecules (Basel, Switzerland) · 2023Review
- Modulation of TRPV1 and TRPA1 Channels Function by Sea Anemones' Peptides Enhances the Viability of SH-SY5Y Cell Model of Parkinson's Disease.International journal of molecular sciences · 2023Article
- Capsaicin alleviates neuronal apoptosis and schizophrenia-like behavioral abnormalities induced by early life stress.Schizophrenia (Heidelberg, Germany) · 2023Article
- KDM4A, involved in the inflammatory and oxidative stress caused by traumatic brain injury-hemorrhagic shock, partly through the regulation of the microglia M1 polarization.BMC neuroscience · 2023Article
- Clcf1/Crlf1a-mediated signaling is neuroprotective and required for Müller glia proliferation in the light-damaged zebrafish retina.Frontiers in cell and developmental biology · 2023Article
- Intestinal Dopamine Receptor D2 is Required for Neuroprotection Against 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Dopaminergic Neurodegeneration.Neuroscience bulletin · 2022Article
- Beneficial Effects of Capsaicin in Disorders of the Central Nervous System.Molecules (Basel, Switzerland) · 2022Review
- Interleukin 13 on Microglia is Neurotoxic in Lipopolysaccharide-injected StriatumExperimental neurobiology · 2022Article
- Natural Products as Novel Neuroprotective Agents; Computational Predictions of the Molecular Targets, ADME Properties, and Safety Profile.Plants (Basel, Switzerland) · 2022Article
- Non-coding RNAs: The Neuroinflammatory Regulators in Neurodegenerative Diseases.Frontiers in neurology · 2022Review
- Ion Channel Dysfunction in Astrocytes in Neurodegenerative Diseases.Frontiers in physiology · 2022Review
- Neuroprotective and Symptomatic Effects of Cannabidiol in an Animal Model of Parkinson's Disease.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
We demonstrated that capsaicin (CAP), an agonist of transient receptor potential vanilloid subtype 1 (TRPV1), inhibits microglia activation and microglia-derived oxidative stress in the substantia nigra (SN) of MPP⁺-lesioned rat. However, the detailed mechanisms how microglia-derived oxidative stress is regulated by CAP remain to be determined. Here we report that ciliary neurotrophic factor (CNTF) endogenously produced by CAP-activated astrocytes through TRPV1, but not microglia, inhibits microglial activation and microglia-derived oxidative stress, as assessed by OX-6 and OX-42 immunostaining and hydroethidine staining, respectively, resulting in neuroprotection. The significant increase in levels of CNTF receptor alpha (CNTFRα) expression was evident on microglia in the MPP⁺-lesioned rat SN and the observed beneficial effects of CNTF was abolished by treatment with CNTF receptor neutralizing antibody. It is therefore likely that CNTF can exert its effect via CNTFRα on microglia, which rescues dopamine neurons in the SN of MPP⁺-lesioned rats and ameliorates amphetamine-induced rotations. Immunohistochemical analysis revealed also a significantly increased expression of CNTFRα on microglia in the SN from human Parkinson's disease patients compared with age-matched controls, indicating that these findings may have relevance to the disease. These data suggest that CNTF originated from TRPV1 activated astrocytes may be beneficial to treat neurodegenerative disease associated with neuro-inflammation such as Parkinson's disease.
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Registered trials
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.