【摘 要】
：
Parkinsons disease (PD) is one of the most common neurodegenerative disorders.Several factors have been implicated as crucial to the pathological mechanism of PD, including mitochondrial dysfunction,o
【机 构】
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Department of Pharmacology,Xuanwu Hospital of Capital Medical University,Beijing,China
【出 处】
：
International Conference for Physiological Sciences 2012(201
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Parkinsons disease (PD) is one of the most common neurodegenerative disorders.Several factors have been implicated as crucial to the pathological mechanism of PD, including mitochondrial dysfunction,oxidative stress, protein aggregation and misfolding, loss of neurotrophic support and apoptosis.In this study, we used l-methyl-4-phenylpyridinium (MPP+)-induced injury in A53T mutant α-synuclein transfected SH-SY5Y cell model, which simulates complex pathological processes of PD, to investigate the apoptotic mechanism of dopaminergic neurons, the relationship of MPP+ and α-synuclein, and the intervention effects and mechanisms of TSG on the above cell model.Results showed that TSG significantly inhibited the MPP-induced mitochondrial apoptotic pathway.TSG also downregulated over-expression of α-synuclein, and regulated the expression of other synaptic proteins to protect the synaptic function.These data indicate the neuroprotective effect of TSG on MPP+-induced injury in A53T mutant a-synuclein transfected SH-SY5Y cell model.It further extended the pharmacological effects of TSG against neurodegenerative diseases, and provided experimental evidence for the treatment of neurodegenerative diseases.
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