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膳食ω-3多不饱和脂肪酸对帕金森病动物模型中毒素诱导的神经元变性的有益作用。

Beneficial effects of dietary omega-3 polyunsaturated fatty acid on toxin-induced neuronal degeneration in an animal model of Parkinson's disease.

作者信息

Bousquet M, Saint-Pierre M, Julien C, Salem N, Cicchetti F, Calon F

机构信息

Centre de Recherche en Endocrinologie Moléculaire et Oncologique, Centre Hospitalier de l'Université Laval, Québec, Canada.

出版信息

FASEB J. 2008 Apr;22(4):1213-25. doi: 10.1096/fj.07-9677com. Epub 2007 Nov 21.

DOI:10.1096/fj.07-9677com
PMID:18032633
Abstract

In this study, we examined whether omega-3 (n-3) polyunsaturated fatty acids (PUFAs) may exert neuroprotective action in Parkinson's disease, as previously shown in Alzheimer's disease. We exposed mice to either a control or a high n-3 PUFA diet from 2 to 12 months of age and then treated them with the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP; 140 mg/kg in 5 days). High n-3 PUFA dietary consumption completely prevented the MPTP-induced decrease of tyrosine hydroxylase (TH)-labeled nigral cells (P<0.01 vs. MPTP mice on control diet), Nurr1 mRNA (P<0.01 vs. MPTP mice on control diet), and dopamine transporter mRNA levels (P<0.05 vs. MPTP mice on control diet) in the substantia nigra. Although n-3 PUFA dietary treatment had no effect on striatal dopaminergic terminals, the high n-3 PUFA diet protected against the MPTP-induced decrease in dopamine (P<0.05 vs. MPTP mice on control diet) and its metabolite dihydroxyphenylacetic acid (P<0.05 vs. MPTP mice on control diet) in the striatum. Taken together, these data suggest that a high n-3 PUFA dietary intake exerts neuroprotective actions in an animal model of Parkinsonism.

摘要

在本研究中,我们检验了ω-3(n-3)多不饱和脂肪酸(PUFA)是否如先前在阿尔茨海默病中所显示的那样,在帕金森病中发挥神经保护作用。我们从2月龄至12月龄将小鼠暴露于对照饮食或高n-3 PUFA饮食中,然后用神经毒素1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP;5天内140 mg/kg)对它们进行处理。高n-3 PUFA饮食完全预防了MPTP诱导的黑质中酪氨酸羟化酶(TH)标记的黑质细胞减少(与对照饮食的MPTP小鼠相比,P<0.01)、Nurr1 mRNA减少(与对照饮食的MPTP小鼠相比,P<0.01)以及多巴胺转运体mRNA水平降低(与对照饮食的MPTP小鼠相比,P<0.05)。尽管n-3 PUFA饮食处理对纹状体多巴胺能终末没有影响,但高n-3 PUFA饮食可防止MPTP诱导的纹状体中多巴胺减少(与对照饮食的MPTP小鼠相比,P<0.05)及其代谢产物二羟基苯乙酸减少(与对照饮食的MPTP小鼠相比,P<0.05)。综上所述,这些数据表明高n-3 PUFA饮食摄入量在帕金森病动物模型中发挥神经保护作用。

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