ArticleNeurotoxicity research2015
A Novel Compound ITC-3 Activates the Nrf2 Signaling and Provides Neuroprotection in Parkinson's Disease Models.
Article in Neurotoxicity research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 25 citations in OpenAlex.
- Nrf2-Keap1 Pathway and NLRP3 Inflammasome in Parkinson's Disease: Mechanistic Crosstalk and Therapeutic Implications.Molecular neurobiology · 2025Review
- Glucosinolate Metabolites and Brain Health: An Updated Review on Their Potential Benefits in Neurodegenerative, Neurodevelopmental, and Psychiatric Disorders.Antioxidants (Basel, Switzerland) · 2025Review
- Novel Sulforaphane Analog Disrupts Phosphatidylinositol-3-Kinase-Protein Kinase B Pathway and Inhibits Cancer Cell Progression via Reactive Oxygen Species-Mediated Caspase-Independent Apoptosis.ACS pharmacology & translational science · 2024Article
- The role of isothiocyanate-rich plants and supplements in neuropsychiatric disorders: a review and update.Frontiers in nutrition · 2024Review
- A Pivotal Role of Nrf2 in Neurodegenerative Disorders: A New Way for Therapeutic Strategies.Pharmaceuticals (Basel, Switzerland) · 2022Review
- A Novel Pyrazolo[3,4-Molecules and cells · 2022Article
- Hydralazine Protects Nigrostriatal Dopaminergic Neurons From MPPFrontiers in neurology · 2019Article
- Neuroprotective Effects and Mechanisms of Action of Multifunctional Agents Targeting Free Radicals, Monoamine Oxidase B and Cholinesterase in Parkinson's Disease Model.Journal of molecular neuroscience : MN · 2017Article
- Isothiocyanates Are Promising Compounds against Oxidative Stress, Neuroinflammation and Cell Death that May Benefit Neurodegeneration in Parkinson's Disease.International journal of molecular sciences · 2016Review
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is a progressive neurodegenerative disorder accompanied by a selective loss of the dopamine(DA)ergic neurons residing in the substantia nigra. There is ample evidence that neuroinflammation and oxidative stress are involved in the pathogenesis of PD. In the present study, we aimed at protecting the DAergic neurons by suppressing these cellular events and generated a novel synthetic isothiocyanate ITC-3. The compound led to elevation of nuclear and total levels of the transcription factor Nrf2 and interacted with its binding protein Keap1 with high affinity, suggesting Nrf2 activation. ITC-3 was able to suppress production of the proinflammatory mediators in lipopolysaccharide-activated BV-2 microglial cells. It also increased mRNA and protein levels of the Nrf2-dependent antioxidant enzymes NAD(P)H quinone oxidoreductase, heme oxygenase-1, and glutamylcysteine ligase in both BV-2 and DAergic neuronal CATH.a cells. The compound protected the DAergic cells against oxidative stress. In vivo, ITC-3 attenuated the loss of tyrosine hydroxylase-immunopositive nigrostriatal DAergic neurons, suppressed microglial activation, and abolished PD-associated motor deficits in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-elicited animal model of PD. Taken together, ITC-3 may be useful toward development of neuroprotective therapy for PD.
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