Koo Jung-Hoon, Cho Joon-Yong, Lee Ung-Bae
Department of Exercise Biochemistry, Korea National Sport University, Seoul 138-763, Republic of Korea; Institute of Sport Science, Korea National Sport University, Seoul, 138-763, Republic of Korea.
Department of Exercise Biochemistry, Korea National Sport University, Seoul 138-763, Republic of Korea.
Exp Gerontol. 2017 Mar;89:20-29. doi: 10.1016/j.exger.2017.01.001. Epub 2017 Jan 4.
Alpha-synuclein (α-Syn) accumulation is significantly correlated with motor deficits and mitochondrial dysfunction in Parkinson's disease (PD), but the molecular mechanism underlying its pathogenesis is unclear. In this study, we investigated the effects of treadmill exercise on motor deficits and mitochondrial dysfunction in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced mouse model of PD. Treadmill exercise inhibited dopaminergic neuron loss by promoting the expression of tyrosine hydroxylase (TH) and dopamine transporter (DAT) and seemed to improve cell survival by reducing α-Syn expression. Most importantly, treadmill exercise increased expression of the mitochondrial import machinery proteins TOM-40, TOM-20, and TIM-23. This was associated with decreased α-Syn expression and subsequent upregulation of the mitochondrial proteins COX-I, COX-IV, and mtHSP70. Taken together, these results indicate that treadmill exercise may ameliorate motor deficits and improve mitochondrial dysfunction by reducing α-Syn expression in the MPTP-induced mouse model of PD.
在帕金森病（PD）中，α-突触核蛋白（α-Syn）的积累与运动功能障碍和线粒体功能障碍显著相关，但其发病机制的分子机制尚不清楚。在本研究中，我们研究了跑步机运动对1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）诱导的PD小鼠模型中运动功能障碍和线粒体功能障碍的影响。跑步机运动通过促进酪氨酸羟化酶（TH）和多巴胺转运体（DAT）的表达来抑制多巴胺能神经元的损失，并且似乎通过降低α-Syn的表达来提高细胞存活率。最重要的是，跑步机运动增加了线粒体导入机制蛋白TOM-40、TOM-20和TIM-23的表达。这与α-Syn表达的降低以及随后线粒体蛋白COX-I、COX-IV和mtHSP70的上调有关。综上所述，这些结果表明，跑步机运动可能通过降低MPTP诱导的PD小鼠模型中的α-Syn表达来改善运动功能障碍并改善线粒体功能障碍。
