基于AMP/ATP-AMPK通路探讨推拿对运动性疲劳大鼠代谢产物蓄积毒性损伤的多靶向调节机制研究

Exercise-induced fatigue is one of the major problems that sports medicine and clinical medicine are currently facing. The key factor relating to sports diseases is the build-up of metabolites during exercise, which causes toxic damage to the central nervous system cells and peripheral skeletal muscle cells. Although tuina (massage therapy), has been used clinically for a long time, to treat exercise-induced fatigue, the onset mechanism is still uncertain. Previous studies found that the high metabolic ability of the meridians can be further stimulated by using corresponding acupoints. Therefore, we propose that tuina (massage therapy) can use this characteristic of the meridians to improve the energy metabolism of human body, promoting the removal o metabolites, hence easing exercise-induced fatigue. On the basis of this hypothesis, we first established mouse models with exercise-induced fatigue. And using molecular biology and immunological methods, we studied the effect of tuina towards the regulating effect of the core regulatory pathway of cell metabolism—AMP/ATP-AMPK and its related factors—LA、BUN、NH3 of peripheral，Na+,K+-ATPase、Ca2+-ATPase of gastrocnemius cells , 5-HT、DA、GABA of cerebral cortex and GnRH of hypothalamus. These prelimary findings of the biological mechanisms behind tuina as a treatment for exercise-induced fatigue, will help establish its clinical value with scientific proof from modern research.

运动疲劳性损伤是当前运动医学与临床医学共同关注的重大问题之一。运动不当引起的代谢产物蓄积，可造成中枢神经细胞及外周骨骼肌细胞的毒性损伤，是导致诸多运动性疾病的关键因素。推拿临床治疗运动疲劳性损伤由来已久，但其作用机制尚未明确。课题组前期工作中发现，经络的高能量代谢特点可通过对相应腧穴的刺激得到进一步表现。因此，我们认为推拿可利用经络的这一特性，改善机体能量代谢水平，促进代谢产物清除，从而缓解运动疲劳性损伤。在此假说的基础上，我们建立了运动性疲劳大鼠模型，采用分子生物学、免疫学的方法，通过研究推拿对运动后细胞能量代谢调控核心通路AMP/ATP-AMPK及其相关因素—外周血LA、BUN、NH3，腓肠肌细胞Na+,K+-ATPase、Ca2+-ATPase，皮层5-HT、DA、GABA及下丘脑GnRH的调节作用，初步揭示推拿治疗运动疲劳性损伤的生物学机制，为其临床应用提供现代科学的试验依据。

运动疲劳性损伤是当前运动医学与临床医学共同关注的重大问题之一。运动不当引起的代谢产物蓄积，可造成中枢神经细胞及外周骨骼肌细胞的毒性损伤，是导致诸多运动性疾病的关键因素。推拿临床治疗运动疲劳性损伤由来已久，但其作用机制尚未明确。课题组前期工作中发现，经络的高能量代谢特点可通过对相应腧穴的刺激得到进一步表现。因此，我们认为推拿可利用经络的这一特性，改善机体能量代谢水平，促进代谢产物清除，从而缓解运动疲劳性损伤。在此假说的基础上，我们建立了运动性疲劳大鼠模型，采用分子生物学、免疫学的方法， 通过研究推拿对运动后细胞能量代谢调控核心通路AMP/ATP-AMPK及其相关因素的调节作用，初步揭示推拿治疗运动疲劳性损伤的生物学机制可能是：推拿手法可以促进运动后代谢产物（如：SOD、MDA、BUN、LAC）的清除，其作用机制可能通过恢复AMP/ATP的平衡，调节AMP/ATP-AMPK信号通路而产生，为其临床应用提供现代科学的试验依据。