中文摘要：

目的：研究消退素D1（Resolvin D1,Rv D1）对非压迫性腰椎间盘突出症模型大鼠背根神经节（dorsal root ganglion,DRG）炎症的影响及内在机制。方法：选取30只雄性大鼠建立非压迫性腰椎间盘突出症模型。随机分为假手术组、模型组、Rv D1组（100 ng）。术后连续3天模型组和Rv D1组分别鞘内注射10μl磷酸盐缓冲液、Rv D1。于术前1天及术后连续7天检测各组大鼠术侧50%缩足阈值（50%paw withdrawal threshold,PWT）。术后第7天,酶联免疫吸附测定术侧L5 DRG中TNF-α和IL-1β的蛋白表达量,免疫组化法检测DRG中p-ERK及NF-κB/p65的阳性表达。结果：术后各时间点,模型组大鼠50%PWT较假手术组明显降低（P〈0.01）;TNF-α和IL-1β表达明显升高（P〈0.01）;p-ERK、NF-κB/p65蛋白水平明显升高（P〈0.01）。术后第2~7天,Rv D1组与模型组相比,50%PWT显著升高（P〈0.05）;TNF-α和IL-1β的蛋白表达明显降低（P〈0.01）;p-ERK及NF-κB/p65蛋白水平明显降低（P〈0.01）。结论：Rv D1促进背根神经节炎症的消退,可能与调节炎症介质TNF-α和IL-1β的表达及ERK和NF-κB/p65通路活性有关。

英文摘要：

Objective： To investigate the therapeutic effects of resolvin D1 on the inflammation of dorsal root ganglion（DRG） and to explore the underlying mechanisms in a non-compressive lumbar disc herniation in the rats. Methods： Non-compressive lumber disc herniation model was established in rats. Rats were randomly divided into three groups： sham group, model group, treatment group（100 ng）（n =10/group）. Intrathecal injection（10 μl） of vehicle or Rv D1（100 ng） was performed for three consecutive days post-operation since the first day after surgery. 50% PWT were evaluated at 1day before and continuous 7 days after operation using the von Frey test. The ipsilateral L5 DRGs were removed and used for measuring expression of proinflammatory cytokines（TNF-α and IL-1β） by ELISA. p-ERK and NF-κB/p65 were measured using immunohistochemistry. Results： Compared with sham group, the vehicle group showed significantly decreased in 50% PWTs during 1~7 days（P〈0.01）, significant increasein expression of TNF-α and IL-1β（P〈0.01） and significant upregulation in p-ERK and NF-κB/p65（P〈0.01）. Compared with that in vehicle group, 50%PWT was significantly increased from the during 2-7 day（P〈0.05） in the Rv D1 group. The expression of TNF-α and IL-1β was significantly decreased（P〈0.01）. Intrathecal injection of Rv D1（100 ng） inhibited the up-regulation of p-ERK and NF-κB/p65（P〈0.01）.Conclusion： This study suggests that intrathecal administration of Rv D1 can alleviate inflammation of DRG probably through regulation of expression of the proinflammatory cytokines and activation of ERK and NF-κB pathways in non-compressive lumbar disc herniation rats.