线粒体
MPTP公司
线粒体呼吸链
药理学
粒线体疾病
呼吸链
细胞凋亡
体内
帕金森病
医学
疾病
生物
病理
线粒体DNA
细胞生物学
生物化学
基因
生物技术
作者
Xianxun Shi,Ming Zhao,Chen Fu,Ailing Fu
出处
期刊:Mitochondrion
[Elsevier]
日期:2017-05-01
卷期号:34: 91-100
被引量:123
标识
DOI:10.1016/j.mito.2017.02.005
摘要
Mitochondrial dysfunction is associated with a large number of human diseases, including neurological and muscular degeneration, cardiovascular disorders, obesity, diabetes, aging and rare mitochondrial diseases. Replacement of dysfunctional mitochondria with functional exogenous mitochondria is proposed as a general principle to treat these diseases. Here we found that mitochondria isolated from human hepatoma cell could naturally enter human neuroblastoma SH-SY5Y cell line, and when the mitochondria were intravenously injected into mice, all of the mice were survived and no obvious abnormality appeared. The results of in vivo distribution suggested that the exogenous mitochondria distributed in various tissues including brain, liver, kidney, muscle and heart, which would benefit for multi-systemically mitochondrial diseases. In normal mice, mitochondrial supplement improved their endurance by increase of energy production in forced swimming test; and in experimental Parkinson's disease (PD) model mice induced by respiratory chain inhibitor MPTP, mitochondrial replacement prevented experimental PD progress through increasing the activity of electron transport chain, decreasing reactive oxygen species level, and preventing cell apoptosis and necrosis. Since effective drugs remain elusive to date for mitochondrial diseases, the strategy of mitochondrial replacement would provide an essential and innovative approach as mitochondrial therapy.
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