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核桃(胡桃仁)在帕金森病模型中的体外和体内神经保护作用

In Vitro and in Vivo Neuroprotective Effects of Walnut (Juglandis Semen) in Models of Parkinson's Disease.

作者信息

Choi Jin Gyu, Park Gunhyuk, Kim Hyo Geun, Oh Dal-Seok, Kim Hocheol, Oh Myung Sook

机构信息

Department of Life and Nanopharmaceutical Sciences, Graduate School, Kyung Hee University, 26 Kyungheedae-ro, Dongdaemun-gu, Seoul 130-701, Korea.

Department of Oriental Pharmaceutical Science, College of Pharmacy and Kyung Hee East-West Pharmaceutical Research Institute, Kyung Hee University, 26 Kyungheedae-ro, Dongdaemun-gu, Seoul 130-701, Korea.

出版信息

Int J Mol Sci. 2016 Jan 15;17(1):108. doi: 10.3390/ijms17010108.

DOI:10.3390/ijms17010108
PMID:26784178
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4730349/
Abstract

Monoamine oxidase (MAO) catalyzes the oxidative deamination of monoamines including dopamine (DA). MAO expression is elevated in Parkinson's disease (PD). An increase in MAO activity is closely related to age, and this may induce neuronal degeneration in the brain due to oxidative stress. MAO (and particularly monoamine oxidase B (MAO-B)) participates in the generation of reactive oxygen species (ROS), such as hydrogen peroxide that are toxic to dopaminergic cells and their surroundings. Although the polyphenol-rich aqueous walnut extract (JSE; an extract of Juglandis Semen) has been shown to have various beneficial bioactivities, no study has been dedicated to see if JSE is capable to protect dopaminergic neurons against neurotoxic insults in models of PD. In the present study we investigated the neuroprotective potential of JSE against 1-methyl-4-phenylpyridinium (MPP⁺)- or 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurotoxicities in primary mesencephalic cells and in a mouse model of PD. Here we show that JSE treatment suppressed ROS and nitric oxide productions triggered by MPP⁺ in primary mesencephalic cells. JSE also inhibited depletion of striatal DA and its metabolites in vivo that resulted in significant improvement in PD-like movement impairment. Altogether our results indicate that JSE has neuroprotective effects in PD models and may have potential for the prevention or treatment of PD.

摘要

单胺氧化酶(MAO)催化包括多巴胺(DA)在内的单胺的氧化脱氨反应。帕金森病(PD)中MAO的表达会升高。MAO活性的增加与年龄密切相关,这可能会因氧化应激导致大脑中的神经元变性。MAO(尤其是单胺氧化酶B(MAO-B))参与活性氧(ROS)的生成,如对多巴胺能细胞及其周围环境有毒的过氧化氢。尽管富含多酚的核桃水提取物(JSE;胡桃种子提取物)已被证明具有多种有益的生物活性,但尚无研究专门探讨JSE是否能够在PD模型中保护多巴胺能神经元免受神经毒性损伤。在本研究中,我们研究了JSE对原代中脑细胞以及PD小鼠模型中1-甲基-4-苯基吡啶鎓(MPP⁺)或1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)诱导的神经毒性的神经保护潜力。在此我们表明,JSE处理可抑制原代中脑细胞中由MPP⁺触发的ROS和一氧化氮的产生。JSE还抑制了体内纹状体DA及其代谢产物的消耗,并显著改善了PD样运动障碍。总之,我们的结果表明JSE在PD模型中具有神经保护作用,可能具有预防或治疗PD的潜力

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