创伤后应激障碍机制的研究进展

Research Progress of Post-traumatic Stress Disorder's Mechanism

创伤后应激障碍(Post-traumatic stress disorder;PTSD)是一种由严重强烈的伤害事件造成的精神障碍,随着近年来社会应激事件的增多和自然灾害的发生,创伤应激障碍的发病率逐渐增高。同时为了研究对应的治疗方法,人们对创伤应激障碍的机制进行了更深入的探索,也有了新的进展。本文着重从激素、神经营养因子、免疫系统等方面来总结创伤后应激障碍发生的生物学机制。激素方面,PTSD主要与交感肾上腺髓质系统(Sympatho-adrenomedullarysystem,SAS)和下丘脑-垂体-肾上腺轴(Hypothalamicpituitary-adrenal axis,HPA)的功能异常有关;神经营养因子方面,其产生与分泌的异常增加或减少可能是PTSD产生的重要机制;免疫系统方面,PTSD可能与免疫系统相关的蛋白质、细胞的数量和功能变化有关。整合神经生物学与分子生物学、表观遗传学、蛋白质组学及分子影像学的成果将对PTSD的研究产生推动作用。

PTSD （Post-traumatic stress disorder） is a mental disorder caused by a seriously intense damage event. Along with the increasing rate of social stress incidents and natural disasters which are common causes of post-traumatic stress disorder （PTSD）, the morbidity of PTSD also rises progressively in recent years. Furthermore, there are many advances of PTSD＇s mechanism made in the ex- ploration of corresponding therapy. We choose some aspects of illustration like hormone, neurotrophic factor, and immunity system to summarize the new improvement of biological mechanism of PTSD. In respect of hormones, PTSD associated with the dysfunction of Sympatho-adrenomedullary-system （SAS） and Hypothalamic-pituitary-adrenal axis （HPA）. The activation of SAS results in calcium over-load in hippocampal neurons which damages the cell membrane and organelle causing function disorders of cell. And abnormal concen-tration of corticotropin-releasing hormone and glucocorticoid inducing peripheral or central symptoms is the effect of dysfunction of HPA. In the aspect of neurotrophic factor, the abnormal increase or decrease of its production and secretion may be the important mecha-nism of PTSD. In the aspect of immunity system, PTSD may be associated with the number and functional changes of the immune-related proteins and cells. Integration of the achievements of neurobiology, molecular biology, epigenetics, proteomics, and molecular imaging will propel the development of PTSD research in the future.