Conclusion: MPTP mice can promote the expression of Parkinson's;
结论：MPTP可促进帕金森模型小鼠表达；
The test prompted that apoptosis attended in mechanisms of PD in MPTP chronic parkinsonism model.
实验结果显示：MPTP慢性帕金森病模型中，细胞凋亡参于了PD的发病机制。
They injected another group of mice with MPTP, a molecule that simulates the effects of Parkinson's disease.
她们对另外一组老鼠注射了MPTP药物，这是一种激发产生帕金森症的分子。
Increasing the expression of that protein in rat neurons grown in culture was enough to reduce the toxic effects of MPTP and rotenone.
在养殖的老鼠神经上增加该蛋白质的显现能够足以降低MPTP和鱼藤酮(rotenone)的毒副作用。
Later, it was learned that MPTP ACTS by interfering with electron transport in mitochondria - a process that is vital for energy generation.
在此之后，研究表明MPTP会干预线粒体的电子传输，而该等电子传输的过程对于能量的制造致关重要。
The overall findings demonstrate that long-term, low-dose exposure to PM alone did not cause signs of neurotoxicity to striatal dopaminergic neural terminals, or enhance the effects of MPTP.
总的说来我们的发现表明长期低剂量PM接触没有单独导致纹状体的多巴胺能的神经末端神经毒性的标志，或者提高了MPTP的作用。
The overall findings demonstrate that long-term, low-dose exposure to PM alone did not cause signs of neurotoxicity to striatal dopaminergic neural terminals, or enhance the effects of MPTP.
总的说来我们的发现表明长期低剂量PM接触没有单独导致纹状体的多巴胺能的神经末端神经毒性的标志，或者提高了MPTP的作用。
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