根性神经痛是椎间盘突出症常见症状，疼痛剧烈，迁延难愈，传统抗炎疗效欠佳。新近研究表明炎症是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，本课题组前期创新性地将“促炎症消退”理念引入到根性神经痛的治疗，在国家自然科学基金资助下对促炎消退介质脂氧素治疗根性神经痛的作用机制进行了深入探讨。研究表明NLRP3炎性小体介导的细胞焦亡在神经系统炎症发生蔓延中起重要作用，而靶向调控细胞焦亡成为治疗多发性硬化等神经系统疾病的新靶点。我们近期实验发现大鼠脊髓背角神经元细胞焦亡参与根性神经痛的发生和发展，而脂氧素B4可抑制细胞焦亡，调控炎症消退而缓解疼痛。本课题将进一步收集临床病例标本，并结合动物及细胞实验，应用siRNA、逆行示踪、免疫荧光、流式细胞分析等技术，探讨脂氧素B4调控细胞焦亡的作用机制，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 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. In our previous study, we have explored the analgesic mechanism of lipoxins for radicular pain founded by National Natural Science Foundation of China(NSFC). Researches prove that pyroptosis mediated by NLRP3 inflammasome is crucial to the enlargement and maintenance of inflammation. And pyroptosis widely participates in the development of inflammatory neurological diseases. Targeting regulation of pyroptosis is expected to be an ideal way for the therapy of neural inflammatory diseases such as multiple sclerosis. In our tentative studies, we found the enlargement of inflammation by neuronal pyroptosis in spinal cord played a key role in radicular pain induced by a rat model of non-compressive lumbar disc herniation. Lipoxin B4 could inhibit pyroptosis and promote inflammatory resolution to relieve radicular pain. This project will further explore the relationship between lipoxins and pyroptosis using siRNA, retrograde tracing, immunofluorescence and other methods to replenish the mechanism of lipoxins in radicular pain therapy from clinical specimens, animal models and cell experiments.