嘌呤能信号和胞外核苷酸酶在疲劳中的作用及机制

疲劳是一种主观不适感，往往表现为多样的躯体和精神主诉，不仅可发展为独立的疾病，也可作为多种疾病中的症状，严重降低人们的生活质量。疲劳的发病机制复杂，近年来，中枢和外周神经递质水平改变和能量代谢异常被认为是主要原因。ATP等嘌呤物质，在细胞内主要参与躯体能量需求过程，而在细胞外则作为重要信号分子，参与有效神经传递、神经元-胶质细胞相互作用、免疫反应和控制等，因而在疲劳研究中受到广泛关注。胞外ATP代谢进一步以浓度依赖的方式激活P1受体和P2受体，而胞外核苷酸酶通过释放受体配体，控制嘌呤物质浓度，以终止或促进嘌呤信号通路。基于此，本文对嘌呤信号和胞外核苷酸酶协同影响疲劳感受与发展进行总结归纳，为深入探讨 疲劳的发病机制并进行有效防治提供依据。

The role and mechanism of purinergic signaling and ecto-nucleotidase in fatigue

Fatigue is a subjective discomfort, often manifested in a variety of physical and mental complaints. It can not only develop into an independent disease, but also as a symptom of a variety of diseases, which seriously reduces people''s quality of life. The pathogenesis of fatigue is complex. In recent years, the changes of central and peripheral neurotransmitter levels and abnormal energy metabolism are considered to be the main causes. Purine substances such as ATP are mainly involved in the process of somatic energy demand, and as important signal molecules, they participate in effective neurotransmission, neuron glial interaction, immune response and control, which have attracted extensive attention in the study of fatigue. Extracellular ATP metabolism further activates P1 receptor and P2 receptor in a concentration dependent manner, while ecto-nucleotidases control the concentration of purine substances by releasing receptor ligands to terminate or promote purine signaling pathway. This paper summarizes the synergistic effects of purine signal and ecto-nucleotidase on the perception and development of fatigue, so as to provide a basis for further discussion on the pathogenesis and effective treatment of fatigue.