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帕金森病实验模型中抗氧化剂神经保护潜力的最新进展。

Recent advances on the neuroprotective potential of antioxidants in experimental models of Parkinson's disease.

作者信息

Koppula Sushruta, Kumar Hemant, More Sandeep Vasant, Kim Byung Wook, Kim In Su, Choi Dong-Kug

机构信息

Department of Biotechnology, Konkuk University, Chungju 380-701, Korea.

出版信息

Int J Mol Sci. 2012;13(8):10608-10629. doi: 10.3390/ijms130810608. Epub 2012 Aug 23.

DOI:10.3390/ijms130810608
PMID:22949883
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3431881/
Abstract

Parkinson's disease (PD), a neurodegenerative movement disorder of the central nervous system (CNS) is characterized by a progressive loss of dopaminergic neurons in the substantia nigra pars compacta region of the midbrain. Although the etiology of PD is not completely understood and is believed to be multifactorial, oxidative stress and mitochondrial dysfunction are widely considered major consequences, which provide important clues to the disease mechanisms. Studies have explored the role of free radicals and oxidative stress that contributes to the cascade of events leading to dopamine cell degeneration in PD. In general, in-built protective mechanisms consisting of enzymatic and non-enzymatic antioxidants in the CNS play decisive roles in preventing neuronal cell loss due to free radicals. But the ability to produce these antioxidants decreases with aging. Therefore, antioxidant therapy alone or in combination with current treatment methods may represent an attractive strategy for treating or preventing the neurodegeneration seen in PD. Here we summarize the recent discoveries of potential antioxidant compounds for modulating free radical mediated oxidative stress leading to neurotoxicity in PD.

摘要

帕金森病(PD)是中枢神经系统(CNS)的一种神经退行性运动障碍,其特征是中脑黑质致密部区域的多巴胺能神经元进行性丧失。尽管PD的病因尚未完全明确,且被认为是多因素的,但氧化应激和线粒体功能障碍被广泛认为是主要后果,这为疾病机制提供了重要线索。研究探讨了自由基和氧化应激在导致PD中多巴胺细胞变性的一系列事件中的作用。一般来说,中枢神经系统中由酶促和非酶促抗氧化剂组成的内在保护机制在防止自由基导致的神经元细胞丢失中起决定性作用。但随着年龄增长,产生这些抗氧化剂的能力会下降。因此,单独使用抗氧化疗法或与当前治疗方法联合使用,可能是治疗或预防PD中所见神经退行性变的一种有吸引力的策略。在此,我们总结了用于调节自由基介导的氧化应激从而导致PD神经毒性的潜在抗氧化化合物的最新发现。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9217/3431881/d056d8873267/ijms-13-10608f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9217/3431881/9296a433d0b7/ijms-13-10608f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9217/3431881/05129729d67c/ijms-13-10608f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9217/3431881/2e75fadf0fb2/ijms-13-10608f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9217/3431881/d056d8873267/ijms-13-10608f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9217/3431881/9296a433d0b7/ijms-13-10608f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9217/3431881/05129729d67c/ijms-13-10608f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9217/3431881/2e75fadf0fb2/ijms-13-10608f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9217/3431881/d056d8873267/ijms-13-10608f4.jpg

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