背景 中枢敏化是持续性疼痛的重要基础机制。活性氧（reactive oxygen species， ROS）为正常细胞代谢的副产品，其表达增加可诱发脊髓中枢敏化参与持续性疼痛。 目的 分析总结ROS在持续性疼痛中枢敏化中作用机制的新近文献资料。 内容 ROS作为中枢敏化过程的功能性信使分子参与持续性疼痛并起关键作用，目前认为其作用机制可能与谷氨酸能通路增强、神经炎症发生、γ-氨基丁酸释放减少和瞬态感受器电位阳离子通道，子类V，成员1（transient receptor potential cation channel， subfamily V， member 1， TRPV1）活化等有关。 趋向 深入研究ROS在中枢敏化中的作用机制将有助于为持续性疼痛提供坚实的治疗策略。
Background Central sensitization is an important mechanism underlying persistent pain. Reactive oxygen species（ROS） are byproducts of normal cellular metabolism. Several studies have suggested that a excess level of ROS can cause central sensitization in the spinal cord leading to persistent pain. Objective To review the recent studies about the roles of ROS in central sensitization underlying persistent pain. Content ROS serve as functional messenger molecules in central sensitization and play a critical role in the development of persistent pain. Alterations in glutamatergic neurotransmission and neuroinflammation， reduction of spinal γ-amino butyric acid release， and modulation of ion channels such as the transient receptor potential cation channel， subfamily V， member 1（TRPV1）， have been proposed as possible mechanisms. Trend Studies concerning the roles of ROS in central sensitization will help the development of solid therapeutic strategies for persistent pain.
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