目的：基于JAK-STAT/SOCS负反馈调节信号通路探讨眩晕方对神经根型颈椎病（cervical spondylotic radiculopathy， CSR）大鼠镇痛作用的机制研究。方法：采用随机、双盲、药物有效治疗对照的方法，构建大鼠急性CSR模型，观察实验动物的行为和体征，进行机械痛阈测定和步态评估。采用酶联免疫吸附实验（enzyme-linked immunosorbent assay，ELISA）法检测脊髓及神经根组织IL-6、PGE2含量；采用免疫共沉淀法检测脊髓组织中SOCS1-JAK1、SOCS3-STAT3蛋白相互作用。结果：假手术组大鼠精神良好、活动灵、足爪未见肿胀、体重增长平稳。造模后大鼠进食明显减少，活动量减低，反应迟钝，毛发暗淡无光，双后足肿胀、溃烂。而治疗组大鼠行为和体征较前改善。相比假手术组，模型组大鼠机械痛阈下降、步态评分升高、IL-6和PGE2水平均显著提升，差异有统计学意义；而治疗组大鼠机械痛阈升高、步态评分降低、IL-6和PGE2水平均显著下降，差异有统计学意义（均P<0.05）。免疫共沉淀结果发现SOCS1和STAT3抗体的条带与input阳性对照条带一致，存在JAK1。结论：眩晕方能够对CSR大鼠具有明显镇痛作用，部分归因于JAK-STAT 信号通路与负反馈因子SOCS直接结合并交互，减少炎症因子表达，从而发挥镇痛作用。本研究从JAK-STAT/SOCS负反馈调节信号通路的新思路出发，为阐明眩晕方对大鼠镇痛作用的机制提供临床循证依据。

Objective: To explore the analgesic mechanism of vertigo prescription on rats with cervical spondylotic radiculopathy (CSR) based on JAK-STAT/SOCS negative feedback regulatory signal pathway. Methods: The acute CSR model of rats was established in the present study on the basis of a randomized, double-blind and effective drug treatment control method. The behavior and signs of experimental animals were performed, associated with mechanical pain threshold measurement and gait assessment. The content of IL-6 and PGE2 in spinal cord and nerve root was detected by enzyme-linked immunosorbent assay (ELISA). The interaction of SOCS1-JAK1 and SOCS3-STAT3 proteins in spinal cord was detected by co-immunoprecipitation. Results: The rats in the sham group had good spirit, no swelling of feet and stable weight growth. After the model was established, the rats ate less, with decreased activity, slow response, dull hair, swollen and festeredhind feet, while the behavior and physical signs of rats were improved in the treatment group. Compared with the sham group, the mechanical pain threshold decreased, gait score increased, IL-6 and PGE2 levels were significantly increased in the model group, the difference was statistically significant (All P<0.05); but in the treatment group, there was increased mechanical pain threshold, decreased gait score, and decreased levels of IL-6 and PGE2 (All P<0.05). The results of Co-Immunoprecipitation showed that the bands in the lysate of SOCS1 and STAT3 antibody were the same as those in the input positive control, with the presence of JAK1. Conclusion: Vertigo prescription has obvious analgesic effect on CSR rats, and its mechanism may be realized by direct interaction between JAK-STAT signal pathway and negative feedback factor SOCS to reduce inflammatory factors and thus to achieve analgesic effect. The present study provides evidence-based clinical basis for clarifying the mechanism of vertigo prescription on analgesia in rats based on JAK-STAT/SOCS negative feedback regulating signal pathway.