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.

中文翻译：

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神经酸改善帕金森病小鼠模型的运动障碍

目的帕金森病（PD）是一种世界范围内常见的神经退行性疾病。先前的研究已经证明从文冠果中提取的神经酸（NA）具有神经保护的潜力。然而，NA 对 PD 的影响仍然未知。本研究旨在探讨NA对运动障碍的潜在功能及其相关机制。方法采用1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)对雄性C57BL/6小鼠产生帕金森运动障碍。进行毒性实验和行为测定来评估 NA 的效果。此外，通过免疫印迹和色谱法探讨体内NA处理后酪氨酸羟化酶和α-突触核蛋白以及纹状体多巴胺（DA）、血清素及其代谢物的表达水平。结果我们发现 NA 可以剂量依赖性地缓解 MPTP 诱导的行为缺陷。而且，NA对小鼠肝脏和肾脏没有毒性作用。值得注意的是，我们发现 NA 显着降低了 MPTP 损伤的影响，而纹状体 DA、血清素和代谢物不受影响。此外，NA处理后，酪氨酸羟化酶上调，而α-突触核蛋白下调，氧化应激受到部分抑制，这可以通过超氧化物歧化酶和谷胱甘肽活性上调来证明。结论 我们的研究结果揭示了 NA 在 PD 小鼠模型中保护运动系统免受运动障碍的潜力，且没有任何副作用，表明 NA 是缓解 PD 症状的替代策略。