目的:研究脊髓白介素33(IL-33)在非压迫性腰椎间盘突出症神经根性疼痛大鼠模型中的作用。方法:选取成年雄性SD大鼠80只，随机分为假手术组、模型组、空载慢病毒组、IL-33重组慢病毒低剂量组、IL-33重组慢病毒高剂量组，每组16只。模型组、空载慢病毒组、IL-33重组慢病毒低剂量组与高剂量组建立非压迫性腰椎间盘突出症模型，假手术组仅暴露手术部位。建模后第3天，模型组、空载慢病毒组、IL-33重组慢病毒低剂量组与高剂量组四组分别鞘内注射感染增强液10 μl、空载慢病毒10 μl、IL-33重组慢病毒混合液5 μl＋感染增强液5 μl、IL-33重组慢病毒混合液10 μl，于建模前1天和建模后第1、3、5、7、9、11、13、15、17、19、21天检测各组大鼠术侧50%缩足阈值(50% PWT)，并在建模后第12天检测脊髓IL-33蛋白和mRNA的表达情况。结果:建模后，模型组和空载慢病毒组大鼠脊髓IL-33蛋白和mRNA的表达量均明显增高(n P<0.01)，而IL-33重组慢病毒低剂量组和高剂量组大鼠脊髓IL-33蛋白和mRNA的表达量较空载慢病毒组显著下降(n P<0.01)。建模后，模型组、空载慢病毒组、IL-33重组慢病毒低剂量组和高剂量组大鼠术侧50% PWT较建模前1天均明显下降(n P<0.01)。建模后第9～21天，IL-33重组慢病毒低剂量组和高剂量组术侧50% PWT较模型组和空载慢病毒组显著升高(n P<0.01)。大鼠脊髓腰段免疫荧光结果显示，相比假手术组，模型组脊髓背角中的IL-33蛋白表达明显增加，而鞘内给予IL-33重组慢病毒5 μl或10 μl均可显著下调脊髓背角中IL-33蛋白的表达。n 结论:腰椎间盘突出髓核可致大鼠脊髓的IL-33表达上调，参与椎间盘源性神经根性疼痛的发生和发展。“,”Objective:To explore the effect of spinal interleutkin-33 (IL-33) on radicular pain in rats modeling non-compressive lumbar disc herniation.Methods:A total of 80 male Sprague-Dawley rats were randomly divided into a sham operation group, a model group, a lentivirus negative control group, a low-dose IL-33 recombinant lentivirus group and a high-dose IL-33 group, each of 16. Non-compressive lumbar disc herniation was successfully induced in all except the rats in the sham operation group. Two days later, the model group was injected intrathecally with 10μl of enhanced infection solution. The lentivirus control group received 10μl of negative lentivirus, the low-dose IL-33 recombinant lentivirus group received 5μl of IL-33 recombinant lentivirus and the high-dose IL-33 recombinant lentivirus group received 10μl of IL-33 recombinant lentivirus. The 50% paw withdrawal threshold (50% PWT) was measured one day before the modeling and on the 1n st, 3n rd, 5n th, 7n th, 9n th, 11n th, 13n th, 15n th, 17n th, 19n th, and 21n st day afterward. On the 12n th day the expressions of IL-33 protein and mRNA were evaluated.n Results:The average expression of IL-33 protein and mRNA in the model and the lentivirus negative control group increased significantly after the modelling compared with the sham group, while expression in the low- and high-dose IL-33 recombinant lentivirus groups was significantly lower than in the lentivirus negative control group. Compared with one day before the modelling, average 50% PWTs on the affected side decreased significantly in all of the modelling groups. From the 9n th to the 21n st day significantly increased 50% PWTs were observed on the affected side in the low-dose and high-dose IL-33 recombinant lentivirus groups compared with the other two modelling groups. Immunostaining showed significant increase in the expression of IL-33 in the dorsal horn of the spinal cord in the model group, compared with the sham operation group. Significant decrease in the average expression of IL-33 in the spinal dorsal horns was observed in the low-dose and high-dose IL-33 recombinant lentivirus groups.n Conclusions:Intervertebral disk herniation may increase the expression of IL-33 in the spinal cord, and may cause radicular pain.