Rifampicin and Parkinson's disease

被引:47
作者
Bi, Wei [1 ,2 ]
Zhu, Lihong [3 ,4 ]
Jing, Xiuna [1 ]
Liang, Yanran [1 ]
Tao, Enxiang [1 ]
机构
[1] Sun Yat Sen Univ, Sun Yat Sen Mem Hosp, Dept Neurol, Guangzhou 510120, Peoples R China
[2] Jinan Univ, Affiliated Hosp 1, Dept Neurol, Guangzhou 510632, Guangdong, Peoples R China
[3] Jinan Univ, Joint Lab Brain Funct & Hlth, Guangzhou 510632, Guangdong, Peoples R China
[4] Jinan Univ, Sch Med, Univ Hong Kong, Guangzhou 510632, Guangdong, Peoples R China
关键词
Rifampicin; Parkinson's disease; Neuroprotection; alpha-Synuclein; Microglial inflammation; Oxidative stress; ALPHA-SYNUCLEIN; OXIDATIVE STRESS; IN-VITRO; PC12; CELLS; AGGREGATION; DAMAGE; BRAIN; MODEL; NEUROTOXICITY; PATHOGENESIS;
D O I
10.1007/s10072-012-1156-0
中图分类号
R74 [神经病学与精神病学];
学科分类号
100204 [神经病学];
摘要
Rifampicin is a macrocyclic antibiotic used extensively for the treatment of Mycobacterium tuberculosis and other mycobacterial infections. Recently, it was discovered that rifampicin exhibits neuroprotective effects. It has been shown to protect PC12 cells against MPP+-induced apoptosis and inhibit the expression of alpha-synuclein multimers. In in vitro studies, rifampicin pretreatment protects PC12 cells against rotenone-induced cell death. Qualitative and quantitative analyses uncover that rifampicin significantly suppresses rotenone-induced apoptosis by ameliorating mitochondrial oxidative stress. It reduces microglial inflammation and improves neuron survival. Our results indicate that rifampicin is cytoprotective under a variety of experimental conditions, and suggest that it may be useful in PD therapeutics. It is the aim of this paper to review the experimental neuroprotection data reported using rifampicin with a focus on the molecular and cellular mechanisms of cytoprotective effect in in vitro models of PD.
引用
收藏
页码:137 / 141
页数:5
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