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氢气对帕金森病动物模型的治疗作用。

Therapeutic effects of hydrogen in animal models of Parkinson's disease.

机构信息

Laboratory of Pathophysiology, Graduate School of Pharmaceutical Sciences, Kyushu University, 3-1-1 Maidashi, Fukuoka 812-8582, Japan.

出版信息

Parkinsons Dis. 2011;2011:307875. doi: 10.4061/2011/307875. Epub 2011 Apr 26.

DOI:10.4061/2011/307875
PMID:21687749
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3109337/
Abstract

Since the first description of Parkinson's disease (PD) nearly two centuries ago, a number of studies have revealed the clinical symptoms, pathology, and therapeutic approaches to overcome this intractable neurodegenerative disease. 1-methy-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 6-hydroxydopamine (6-OHDA) are neurotoxins which produce Parkinsonian pathology. From the animal studies using these neurotoxins, it has become well established that oxidative stress is a primary cause of, and essential for, cellular apoptosis in dopaminergic neurons. Here, we describe the mechanism whereby oxidative stress evokes irreversible cell death, and propose a novel therapeutic strategy for PD using molecular hydrogen. Hydrogen has an ability to reduce oxidative damage and ameliorate the loss of nigrostriatal dopaminergic neuronal pathway in two experimental animal models. Thus, it is strongly suggested that hydrogen might provide a great advantage to prevent or minimize the onset and progression of PD.

摘要

自近两个世纪前首次描述帕金森病(PD)以来,许多研究已经揭示了这种难治性神经退行性疾病的临床症状、病理学和治疗方法。1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)和 6-羟多巴胺(6-OHDA)是产生帕金森病病理学的神经毒素。从使用这些神经毒素的动物研究中可以清楚地看出,氧化应激是多巴胺能神经元细胞凋亡的主要原因和必要条件。在这里,我们描述了氧化应激引发不可逆转的细胞死亡的机制,并提出了一种使用分子氢治疗 PD 的新的治疗策略。氢具有减轻氧化损伤的能力,并在两种实验动物模型中改善黑质纹状体多巴胺能神经元通路的丧失。因此,强烈建议氢可能提供很大的优势,以预防或最小化 PD 的发作和进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df48/3109337/fcfd98f44437/PD2011-307875.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df48/3109337/8665ee80fef6/PD2011-307875.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df48/3109337/fcfd98f44437/PD2011-307875.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df48/3109337/8665ee80fef6/PD2011-307875.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df48/3109337/fcfd98f44437/PD2011-307875.002.jpg

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