我们前期研究发现线粒体相关的自噬在预运动训练延缓PD发病过程中发挥了重要作用。本研究拟在此基础上，进一步分析机体在应对MPTP毒性机制过程中自噬与凋亡平衡的动态变化，及其与线粒体稳态之间的关系。建立两种早期运动（抗阻和耐力）干预PD发病小鼠模型，从自噬与凋亡平衡的角度，以肌肉因子IL-15为切入点，观察运动运动诱导的肌源性IL-15对PD模型小鼠中脑和纹状体的远程调控作用，及其与年龄因素的交互影响。通过电刺激C2C12肌管细胞，取培养液孵育PC12细胞，在细胞水平上模拟预运动对PD模型的影响，同时应用RNAi IL-15，RNAi PGC-1α等干预手段，进一步研究IL-15作用机制；选取野生小鼠和IL15-/-小鼠进行抗阻运动，分别注射IL-15阻断剂和IL-15，再次论证IL-15作为信使分子介导骨骼肌与脑cross-talk的研究假设，为运动延缓PD发病的提供新的思路和直接的理论依据

Parkinson's disease (PD) is a neurodegenerative disease which is a serious threat to the elder group. Our previous study have found that enhanced autophagy levels induced by mitochondrial played an important role in the protective process of prior -exercise training on PD. These studies will analysis the changes of balance between autophagy and apoptosis in the mouse model response to the MPTP toxicity. The resistance- and endurance-type exercise intervention models in mouse are built to observe the remote-control role of muscle-derived IL-15 on brain and striatum of PD mouse, and its interaction with the age factor, from the point of view of the balance between autophagy and apoptosis. Cell model is built by electrical stimulation of C2C12 myotubes and incubation the PC12 cells with the culture medium. Intervention means of the RNAi IL-15, RNAi PGC-1α and blockers added to C2C12 were used to further study the mechanism of IL-15 action. Injection of blocker of IL-15 and IL-15 to the wild-type and IL15-/- mice correspondingly after resistance training are devised to further demonstrate the hypothesis that IL-15 as a messenger molecule mediate the cross-talk between skeletal muscle and brain.The study will provide new ideas and direct theoretical basis for the neuroprotective role of the prior exercise training on the PD.