ArticleFrontiers in immunology2021
Dl-3-n-Butylphthalide Rescues Dopaminergic Neurons in Parkinson's Disease Models by Inhibiting the NLRP3 Inflammasome and Ameliorating Mitochondrial Impairment.
Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 107 citations in OpenAlex.
- Cognitive-Motor Dual Task Training Synergistically Improves Aging-related Cognitive Dysfunction By Reducing TMAO and Suppressing TXNIP/NLRP3 Pathway.Molecular neurobiology · 2026Article
- Identification of hypertension-associated bacterial key genes as potential targets and therapeutic agents through integrated bioinformatics approach.International microbiology : the official journal of the Spanish Society for Microbiology · 2026Article
- Hirudin as a Therapeutic and Brain-Delivery Platform: From Stroke to Central Nervous System Disorders.International journal of molecular sciences · 2026Review
- DL-3-n-Butylphthalide Protects Against PrPCNS neuroscience & therapeutics · 2026Article
- Icaritin ameliorates MPTP-induced Parkinson's disease model by targeting the NLRP3 inflammasome pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Sources of Oxidative Stress in Parkinson's Disease: Pathways and Therapeutic Implications.Antioxidants (Basel, Switzerland) · 2026Review
- 3-n-Butylphthalide Protects SH-SY5Y Cells from Ferroptosis by Inhibiting ACSL4-Mediated Lipid Peroxidation.Molecular neurobiology · 2026Article
- Organelle stress in NLRP3 inflammasome: a central mediator of neurodegenerative diseases.Molecular neurodegeneration · 2026Review
- The NLRP3-α-Synuclein Circuit: A Core Driver and Therapeutic Target in Parkinson's Disease.Journal of inflammation research · 2026Review
- DL-3-n-Butylphthalide Protects Mitochondria Against Ischemia/Hypoxia Damage via Suppressing GCN5L1-Mediated Drp1 Acetylation in Neurons and Mouse Brains.CNS neuroscience & therapeutics · 2025Article
- Inhibiting TRPV4 improves α-synuclein degradation through autophagy-lysosomal pathway in the MPPScientific reports · 2025Article
- Cellular fibronectin exacerbates α-synuclein aggregation via integrin alpha4beta1 mediated PARP1 and SCD elevation.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Palmatine Ameliorates Motor Deficits and Dopaminergic Neuron Loss by Regulating NLRP3 Inflammasome through Mitophagy in Parkinson's Disease Model Mice.Molecular neurobiology · 2025Article
- Targeting NLRP3 Inflammasomes: A Trojan Horse Strategy for Intervention in Neurological Disorders.Molecular neurobiology · 2025Review
- Neuroprotective Effects of Myrtle Berry By-Product Extracts on 6-OHDA-Induced Cytotoxicity in PC12 Cells.Antioxidants (Basel, Switzerland) · 2025Article
- Butylphthalide reduces plaque burden and improves neurological function in carotid atherosclerotic disease: a pooled analysis.Frontiers in pharmacology · 2025Article
- Dual role of exosomes in neurodegenerative diseases: a molecular bridge between neuroinflammation and transmission of pathological proteins.Frontiers in neurology · 2025Review
- Article
- Dl-3-n-butylphthalide attenuates DOX-induced cardiotoxicity in mice by inhibiting Nrf2/Keap1 complex formation.Frontiers in pharmacology · 2025Article
- Mitochondrial quality control and transfer communication in neurological disorders and neuroinflammation.Frontiers in immunology · 2025Review
3 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Neuroinflammation and mitochondrial impairment play important roles in the neuropathogenesis of Parkinson's disease (PD). The activation of NLRP3 inflammasome and the accumulation of α-synuclein (α-Syn) are strictly correlated to neuroinflammation. Therefore, the regulation of NLRP3 inflammasome activation and α-Syn aggregation might have therapeutic potential. It has been indicated that Dl-3-n-butylphthalide (NBP) produces neuroprotection against some neurological diseases such as ischemic stroke. We here intended to explore whether NBP suppressed NLRP3 inflammasome activation and reduced α-Syn aggregation, thus protecting dopaminergic neurons against neuroinflammation. Methods: In our study, we established a MPTP-induced mouse model and 6-OHDA-induced SH-SY5Y cell model to examine the neuroprotective actions of NBP. We then performed behavioral tests to examine motor dysfunction in MPTP-exposed mice after NBP treatment. Western blotting, immunofluorescence staining, flow cytometry and RT-qPCR were conducted to investigate the expression of NLRP3 inflammasomes, neuroinflammatory cytokines, PARP1, p-α-Syn, and markers of microgliosis and astrogliosis. Results: The results showed that NBP exerts a neuroprotective effect on experimental PD models. Conclusions: In summary, NBP rescued dopaminergic neurons by reducing NLRP3 inflammasome activation and ameliorating mitochondrial impairments and increases in p-α-Syn levels. This current study may provide novel neuroprotective mechanisms of NBP as a potential therapeutic agent.
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