应激反应或疼痛的持续存在是机体对外界不良刺激反应的结果,最终导致健康受损。疼痛和应激反应相互影响,改变了机体的稳态。胶质细胞(glial cells)活化是慢性应激和慢性疼痛发生发展的共同病理基础。本文对胶质细胞在慢性应激和慢性疼痛间的关联作用及其机制研究进展进行综述。胶质细胞的激活是慢性应激诱发疼痛的主要特征和驱动因素之一,激活后的胶质细胞通过MAPK信号通路、趋化因子和炎性因子及相关受体等一系列机制诱发痛觉敏化,神经元-胶质细胞相互作用调节慢性应激诱发的疼痛。胶质细胞的生理和病理变化与一些慢性应激诱发的临床疾病的发生密切相关。

The persistence of stress responses or pain is a consequence of the body's reaction to adverse external stimuli, ultimately leading to maladaptation. The interactions between stress responses and pain challenge the body’s homeostasis. The review summarizes the research progress on the interrelated roles and mechanisms of glial cells in chronic stress and pain. Glial cell activation is one of the main features and driving factors of chronic stress-induced pain. Activated glial cells are involved in pain sensitization through a series of mechanisms, including the MAPK signaling pathway, chemokines, cytokines, and related receptors. Meanwhile, neuron-glial interactions regulate chronic stress-induced pain. The physiological and pathological changes in glial cells are closely related to the onset of some diseases induced by chronic stress.