【目的】 观察夹脊电针对脊髓损伤大鼠的治疗作用及机制。【方法】 将48只SD大鼠随机分为假手术组、模型组、夹脊 电针组、夹脊电针＋单钠尿酸盐（MSU）[NOD样受体热蛋白结构域相关蛋白3（NLRP3）激活剂]组，每组分为3、7 d两个亚组， 每个时间点6只大鼠。除假手术组，其他各组大鼠采用改良Allen’s法制备脊髓损伤模型。夹脊电针组大鼠取双侧T9、T11夹 脊穴电针治疗。夹脊电针＋MSU组腹腔注射MSU，再进行夹脊穴电针治疗。分别治疗3、7 d后取材。采用BBB评分评价大 鼠运动功能，苏木精-伊红（HE）染色法观察各组大鼠脊髓组织病理形态，免疫荧光双标法检测大鼠离子钙接头蛋白1（Iba-1） 与M1小胶质细胞标志物诱导型一氧化氮合酶（iNOS）以及Iba-1与M2小胶质细胞标志物精氨酸酶1（Arg-1）在脊髓组织中的表 达及定位情况。进一步采用Western Blot法检测大鼠脊髓组织Iba-1、iNOS、Arg-1、白细胞介素1β（IL-1β）的蛋白表达水平。 【结果】（1）与假手术组比较，模型组大鼠于干预3、7 d时BBB评分降低（P＜0.05）；与模型组比较，夹脊电针组于干预3、7 d BBB评分升高（P＜0.05）；夹脊电针+MSU组 BBB评分低于夹脊电针组。（2）模型组大鼠脊髓组织可见出血区，并有炎性细胞 浸润；夹脊电针组脊髓组织炎性细胞浸润减少。（3）与假手术组比较，模型组 Iba-1与 iNOS共表达荧光强度升高（P＜0.05）， Iba-1 与 Arg-1 共表达荧光强度下降（P＜0.05）；与模型组比较，夹脊电针组 2 个时间点 Iba-1 与 iNOS 共表达荧光强度降低 （P＜0.05），Iba-1与 Arg-1共表达荧光强度升高（P＜0.05）。MSU 干预对电针治疗效果有抑制作用。（4）与假手术组比较，模 型组Iba-1、iNOS、IL-1β的蛋白表达水平升高（P＜0.05），Arg-1蛋白表达水平下降（P＜0.05）；与模型组比较，夹脊电针组 脊髓组织Iba-1、iNOS、IL-1β蛋白表达水平降低（P＜0.05），Arg-1蛋白表达水平升高（P＜0.05）。【结论】 夹脊电针能够提高 脊髓损伤大鼠运动功能，其机制可能与调控NLRP3继而抑制小胶质细胞M1极化及炎性物质释放、促进M2极化有关。

Objective To observe the therapeutic effect of electroacupuncture （EA） at Jiaji points （EX-B2） on rats with spinal cord injury （SCI） and to explore its underlying mechanism. Methods Forty-eight SD rats were randomly divided into a sham-operated group， a model group， a Jiaji EA group， and a Jiaji EA + NLRP3 activator monosodium urate （MSU） group. Each group was further divided into two subgroups （3-day and 7-day time points，n=6 per subgroup）. SCI was induced in all groups except the sham-operated group using the modified Allen’s method. The Jiaji EA group received electroacupuncture at bilateral T9 and T11 of Jiaji points. The Jiaji EA + MSU group received intraperitoneal MSU injection prior to Jiaji EA treatment. Tissue samples were collected after 3 and 7 days of treatment. The Basso，Beattie，Bresnahan （BBB） scale was used to assess rat motor function， hematoxylin-eosin （HE） staining was performed to observe histopathological changes in spinal cord tissue， and immunofluorescence double labeling was used to detect the expression and localization of ionized calcium-binding adapter molecule 1（Iba-1） with the M1 microglial marker inducible nitric oxide synthase （iNOS），and Iba-1 with the M2 microglial marker arginase-1（Arg-1） in spinal cord tissue. Western Blot was further used to measure protein expression levels of Iba-1，iNOS，Arg-1，and interleukin-1β（IL-1β） in the spinal cord tissue. Results （1） Compared with the sham-operated group，the BBB scores of the model group were significantly decreased at 3 and 7 days post-of intervention （P＜0.05）. Compared with the model group，the BBB scores of the Jiaji EA group were significantly increased at both time points （P＜0.05）. The BBB scores of the Jiaji EA + MSU group were lower than those of the Jiaji EA group.（2） Hemorrhagic areas and inflammatory cell infiltration were observed in the spinal cord tissue of the model group，while inflammatory cell infiltration was reduced in the Jiaji EA group. （3）Compared with the sham-operated group， the model group showed increased fluorescence co-expression intensity of Iba-1 and iNOS （P＜0.05） and decreased co-expression intensity of Iba-1 and Arg-1（P＜0.05）. Compared with the model group，the co-expression intensity of Iba-1 and iNOS was decreased in the Jiaji EA group （P＜0.05），while the co-expression intensity of Iba-1 and Arg-1 was increased （P＜0.05） at both time points. Administration of the agonist （MSU） inhibited the therapeutic effect of electroacupuncture.（4）Compared with the sham-operated group，the model group exhibited increased protein expression levels of Iba-1，iNOS， and IL-1β（P＜0.05） and decreased Arg-1 protein expression （P＜0.05）. Compared with the model group，the protein expression levels of Iba-1，iNOS，and IL-1β were significantly decreased in the Jiaji EA group （P＜ 0.05），while Arg-1 protein expression was significantly increased （P＜0.05）. Conclusion EA at Jiaji points can improve motor function in rats with SCI，and its mechanism may be related to the regulation of NLRP3，thereby inhibiting M1 microglial polarization and inflammatory mediator release，and promoting M2 polarization.

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国家自然科学基金项目（编号：81774427）；国家中医药管理局高水平中医药重点学科建设项目（编号：14061230010）