根性神经痛是椎间盘突出症患者常见症状，疼痛剧烈，迁延难愈。突出髓核造成的神经根炎性反应是根性神经痛的重要致病机制，但传统的抗炎治疗效果欠佳。新近发现炎症是一个从启动到消退的主动化过程，炎症消退过程亦由内源性化学介质主动调控。基于此，本课题组将“促炎症消退”这一全新理念引入到椎间盘突出症的治疗中，在国家自然科学基金面上项目资助下研究了促炎消退介质脂氧素治疗根性神经痛的作用机制。补体系统是免疫炎症反应的重要组成部分，我们研究中新发现模型大鼠中失调的补体系统打破了神经根炎症产生与消退的动态平衡，而鞘内注射脂氧素对过度激活的补体系统有负向调节作用。因此本课题组拟从整体、细胞及分子等不同水平，应用siRNA、Western blot、免疫荧光、胶体金免疫电镜、激光共聚焦等技术，深入探讨非压迫性椎间盘突出症大鼠模型中脂氧素参与调控补体系统的作用机制，进一步完善促炎症消退介质治疗根性神经痛的理论体系。

Radicular pain, or radiculitis, is pain that experienced along the dermatome (or sensory distribution) of a nerve due to stimulation on the nerve root and is hardly to be cured. The most common cause of radicular pain is intervertebral disc herniation and its mechanism is still not well understood. Reports have demonstrated that inflammatory response induced by protrused nucleus pulposus plays a key role in the process of radicular pain. But anti-inflammatory therapy for the radicular pain did not produce good results. In recent years, it has been proved that the resolution of inflammation is an active programmed process regulated by pro-resolving lipid mediators, such as lipoxins, resolvins et al. In our previous study, we have explored the analgesic mechanism of lipoxins for radicular pain. Complement system participates in inflammatory process, and disregulated complement system breaks the balance between production and resolution of inflammation. We have initially found complement system was regulated by lipoxins. In our tentative studies, the expressions of C3,C5a and C3aR were up-regulated in a rat model of non-compressive lumbar disc herniation. Intrathecal administration of lipoxinA4 (100ng) reduced the expression of C3aR protein and enhanced the expression of regulatory protein CD55. This project will further explore the relationship between lipoxins and complement system using siRNA, immunofluorescence, immuno-electron microscope, HPLC-MS, laser confocal microscopy, western blot and other methods to replenish the mechanism of lipoxins in radicular pain therapy.