慢性疼痛的细胞因子微环境假说

CYTOKINE MICROENVIRONMENT HYPOTHESIS OF CHRONIC PAIN

慢性疼痛常常伴有记忆和情感障碍,严重影响患者的生活质量和工作能力,但目前慢性疼痛机制不清。慢性疼痛常常伴有神经系统致炎细胞因子异常升高,在外周神经或中枢施以致炎细胞因子可模拟神经损伤引起的慢性疼痛和记忆情感障碍。根据致炎细胞因子可模拟神经损伤,持久改变神经元的兴奋性和突触可塑性,我们提出慢性疼痛细胞因子微环境假说,即,在神经损伤等强伤害性刺激的作用下,神经系统细胞因子微环境发生异常改变,即致炎细胞因子升高,抗炎细胞因子减少,导致神经系统的结构和功能发生变化,引起慢性疼痛及其相伴的认知和情感障碍。防止或纠正细胞因子微环境的失衡可能从根本上预防和治疗慢性疼痛。

Chronic pain is often accompanied by memory defcits and affective disorders which seriously affect patients＇ life quality and working ability,however,underlying mechanisms of chronic pain are poorly understood.Chronic pain is often accompanied by abnormal increase of proinflammatory cytokines in nervous system.Administration of proinflammatory cytokines to peripheral nerves or central nerves can simulate chronic pain,memory and mood disorders induced by nerve damage.Hence,according to the fact that proinfammatory cytokines can simulate nerve damage and sustainedly change neuron excitability and synaptic plasticity,we suggested a cytokine microenvironment hypothesis of chronic pain,i.e.,strong noxious stimulation such as nerve injury might induce abnormal change of cytokine microenvironment in nervous system,in such circumstance,an increase in proinfammatory cytokine and a decrease in antiinflammatory ones may lead to chronic pain and its accompanied cognitive and affective disorders by altering the function and structure of nervous system.Thus,blockage or correction of the abnormal change in cytokine microenvironment may fundamentally prevent or cure chronic pain.