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Nervonic acid amends motor disorder in a mouse model of Parkinson’s disease
OBJECTIVES: Parkinson’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...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
De Gruyter
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8149914/ https://www.ncbi.nlm.nih.gov/pubmed/34055392 http://dx.doi.org/10.1515/tnsci-2020-0171 |
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author | Hu, Dandong Cui, Yujuan Zhang, Ji |
author_facet | Hu, Dandong Cui, Yujuan Zhang, Ji |
author_sort | Hu, Dandong |
collection | PubMed |
description | OBJECTIVES: Parkinson’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. METHODS: 1-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. RESULTS: We 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. CONCLUSION: Our 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. |
format | Online Article Text |
id | pubmed-8149914 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | De Gruyter |
record_format | MEDLINE/PubMed |
spelling | pubmed-81499142021-05-28 Nervonic acid amends motor disorder in a mouse model of Parkinson’s disease Hu, Dandong Cui, Yujuan Zhang, Ji Transl Neurosci Research Article OBJECTIVES: Parkinson’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. METHODS: 1-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. RESULTS: We 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. CONCLUSION: Our 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. De Gruyter 2021-05-25 /pmc/articles/PMC8149914/ /pubmed/34055392 http://dx.doi.org/10.1515/tnsci-2020-0171 Text en © 2021 Dandong Hu et al., published by De Gruyter https://creativecommons.org/licenses/by/4.0/This work is licensed under the Creative Commons Attribution 4.0 International License. |
spellingShingle | Research Article Hu, Dandong Cui, Yujuan Zhang, Ji Nervonic acid amends motor disorder in a mouse model of Parkinson’s disease |
title | Nervonic acid amends motor disorder in a mouse model of Parkinson’s disease |
title_full | Nervonic acid amends motor disorder in a mouse model of Parkinson’s disease |
title_fullStr | Nervonic acid amends motor disorder in a mouse model of Parkinson’s disease |
title_full_unstemmed | Nervonic acid amends motor disorder in a mouse model of Parkinson’s disease |
title_short | Nervonic acid amends motor disorder in a mouse model of Parkinson’s disease |
title_sort | nervonic acid amends motor disorder in a mouse model of parkinson’s disease |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8149914/ https://www.ncbi.nlm.nih.gov/pubmed/34055392 http://dx.doi.org/10.1515/tnsci-2020-0171 |
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