Abstract
ObjectivesParkinson’s disease (PD) is a kind of common neurodegenerative disease in the world. Previous studies have proved that nervonic acid (NA), extracted from Xanthoceras sorbifolia Bunge, has the potentials of neuroprotection. However, the effect of NA on the PD remained unknown. This study was designed to investigate the NA’s potential function and relative mechanism on motor disorder.Methods1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was used for producing parkinsonism motor disorder on male C57BL/6 mice. Toxicity experiments and behavioral assay were performed to evaluate the effect of NA. Besides, the expression levels of tyrosine hydroxylase and α-synuclein, as well as striatal dopamine (DA), serotonin, and their metabolites were explored through immunoblotting and chromatography after NA treatment in vivo.ResultsWe found that NA could alleviate the MPTP-induced behavioral deficits dose-dependently. Moreover, NA has no toxic effects on the mouse liver and kidney. Of note, we found that NA significantly reduced the impact of MPTP impairment and striatal DA, serotonin, and metabolites were remained unaffected. In addition, tyrosine hydroxylase was upregulated while α-synuclein being downregulated and the oxidative stress was partially repressed evidenced by the upregulation of superoxide dismutase and glutathione activity after NA treatment.ConclusionOur findings unveil NA’s potential for protecting motor system against motor disorder in the PD mouse model without any side effects, indicating NA as an alternative strategy for PD symptom remission.
Highlights
Parkinson’s disease (PD), as the second grave health problem of neurodegenerative diseases, is affecting about 3% of the population aged over 60 [1]
The control group was treated by vehicle without MPTP stimulation
The number of spontaneous movements increased from 75.61 ± 8.33 turns/min to 87.31 ± 7.8 turns/min. Only those treated with a high dose of nervonic acid (NA) (>40 mg/kg) presented a significant difference compared to the model group (p < 0.05)
Summary
Parkinson’s disease (PD), as the second grave health problem of neurodegenerative diseases, is affecting about 3% of the population aged over 60 [1]. Serotonin (5-HT) is highlighted to be a novel marker of PD [6] Based on these mechanisms, several therapy strategies are investigated to alleviate or suppress this neurodegenerative disease, among which DA supplementation with drugs, including L-3,4-dihydroxyphenylalanine (L-DOPA), DA agonist, and monoamine oxidase B (MAO-B) inhibitors [7], is used to inhibit DA breakdown or activate DA receptor. Several therapy strategies are investigated to alleviate or suppress this neurodegenerative disease, among which DA supplementation with drugs, including L-3,4-dihydroxyphenylalanine (L-DOPA), DA agonist, and monoamine oxidase B (MAO-B) inhibitors [7], is used to inhibit DA breakdown or activate DA receptor These treatments may cause various severe side effects and drug resistance. Nondopaminergic therapies, such as inosine, iron chelators, and anti-inflammatories, as well as non-pharmacological approaches (e.g., gene therapies and neurotrophic factors) have been strongly supported by pre-clinic studies [8,9], while no approach has convincingly showed the advancement in the clinic
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
