Journal
NEUROCHEMICAL JOURNAL
Volume 15, Issue 3, Pages 317-324Publisher
MAIK NAUKA/INTERPERIODICA/SPRINGER
DOI: 10.1134/S1819712421030065
Keywords
Parkinson's disease; nervonic acid; motor disorder
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The study demonstrated that NA dose-dependently alleviated MPTP-induced behavioral deficits and had no toxic effects on the mouse liver and kidney. Furthermore, NA significantly restored striatal dopamine, serotonin, and their metabolites.
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 alpha-synuclein, as well as striatal dopamine, 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 restored striatal dopamine, serotonin, and metabolites. In addition, tyrosine hydroxylase was upregulated while alpha-synuclein being downregulated and the oxidative stress was partially repressed evidenced by the upregulation of superoxide dismutase (SOD) and glutathione (GSH) 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.
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