ArticleMolecular neurobiology2018
N-Propargyl Caffeamide (PACA) Ameliorates Dopaminergic Neuronal Loss and Motor Dysfunctions in MPTP Mouse Model of Parkinson's Disease and in MPP
Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 37 citations in OpenAlex.
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- Physical Exercise and Health: A Focus on Its Protective Role in Neurodegenerative Diseases.Journal of functional morphology and kinesiology · 2022Review
- HOTTIP downregulation reduces neuronal damage and microglial activation in Parkinson's disease cell and mouse models.Neural regeneration research · 2022Article
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- A Study on THE Mechanism of Electroacupuncture to Alleviate Visceral Pain and NGF Expression.Computational intelligence and neuroscience · 2022Article
- A Novel Synthetic Precursor of Styryl Sulfone Neuroprotective Agents Inhibits Neuroinflammatory Responses and Oxidative Stress Damage through the P38 Signaling Pathway in the Cell and Animal Model of Parkinson's Disease.Molecules (Basel, Switzerland) · 2021Article
- Partial depletion and repopulation of microglia have different effects in the acute MPTP mouse model of Parkinson's disease.Cell proliferation · 2021Article
- Article
- Neuroprotection Against Parkinson's Disease Through the Activation of Akt/GSK3β Signaling Pathway by Tovophyllin A.Frontiers in neuroscience · 2020Article
- Botanical Drug Puerarin Promotes Neuronal Survival and Neurite Outgrowth against MPTP/MPPOxidative medicine and cellular longevity · 2020Article
- Neuroprotective effects of protocatechuic aldehyde through PLK2/p-GSK3β/Nrf2 signaling pathway in bothAging · 2019Article
- Review
- Electro-Acupuncture Ameliorated MPTP-Induced Parkinsonism in Mice via TrkB Neurotrophic Signaling.Frontiers in neuroscience · 2019Article
- Effects of Combined Treatment with Acupuncture and Chunggan Formula in a Mouse Model of Parkinson's Disease.Evidence-based complementary and alternative medicine : eCAM · 2019Article
- Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Insufficient production of nerve growth factor (NGF) is implicated in Parkinson's disease (PD). We recently discovered that caffeic acid derivative N-propargyl caffeamide (PACA) not only potentiated NGF-induced neurite outgrowth but also attenuated 6-hydroxydopamine neurotoxicity in neuronal culture. The aim of the present study was to investigate whether PACA could increase NGF levels against 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) neurotoxicity in a mouse PD model. We induced parkinsonism in mice by intraperitoneal injection of MPTP for seven consecutive days. Animal motor functions were assessed by rotarod test and pole test. Our results showed that PACA ameliorated motor impairments in MPTP-challenged mice. Based on Western blot analysis and/or immunofluorescence staining of NGF and tyrosine hydroxylase (TH), PACA preserved TH levels in the midbrain substantia nigra pars compacta. PACA also increased NGF expression while it decreased proNGF accumulation. Interestingly, NGF was widely induced in the midbrains including astrocytes. To elucidate the mechanisms by which PACA induces NGF, we focused on the effects of PACA on two neurotrophic signaling pathways, the PI3K and MEK pathways. We found that PACA induced the phosphorylation of Akt, ERK, and CREB against MPTP-mediated alterations. Importantly, PACA increased NGF levels and subsequently induced TrkA activation in MPTP-treated mice. Consistently, PACA also increased NGF levels in dopaminergic PC12 cells and primary rat midbrain neurons against N-methyl-4-phenylpyridinium iodide (MPP
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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.