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目的:探讨趋化因子配体2(chemokine C-C motif ligand 2，CCL2)及其受体在臂丛神经根性撕脱伤(brachial plexus avulsion，BPA)诱发神经病理性痛(neuropathic pain，NP)中的作用机制。方法:将30只大鼠随机分为空白对照组(sham)、BPA-NP模型+生理盐水组、BPA-NP模型+CCR2抑制剂组、BPA-NP模型+JAK抑制剂组、BPA-NP模型+NR2B抑制剂组。建立大鼠臂丛神经下干撕脱伤(BPA-NP)模型，分别检测各组大鼠颈n 8-胸n 1节段脊髓背角区域CCL2及其受体CCR2的表达。同时通过Western Blot检测各组大鼠颈n 8-胸n 1节段脊髓背角区域CCL2、CCR2、NR2B的表达。n 结果:BPA-NP模型+生理盐水组大鼠颈n 8-胸n 1节段脊髓背角CCL2及CCR2的荧光定量及蛋白表达量较BPA-NP模型+CCR2抑制剂干预组及空白对照组显著升高，差异具有统计学意义；加入CCR2、JAK及NR2B抑制剂并不能完全抑制CCL2及CCR2的表达，也不能完全抑制NR2B的表达。n 结论:外伤因素会导致BPA-NP大鼠颈n 8-胸n 1节段脊髓背角CCL2表达增高，进而与其受体CCR2结合通过激活下游JAK/STAT信号通路但并非唯一通路引起NMDA受体NR2B表达上调，增强中枢敏化作用导致NP的发生。CCL2-JAK/STAT-NMDA通路可能是BPA诱发NP的机制之一。n “,”Objective:To investigate the mechanism of chemokine (C-C motif) ligand 2 (CCL2) and its receptors in neuropathic pain (NP) induced by brachial plexus avulsion (BPA).Methods:Thirty rats were randomly divided into 5 groups, including blank control group (sham), BPA-NP model+ saline group, BPA-NP model+ CCR2 inhibitor group, BPA-NP model+ JAK inhibitor group and BPA-NP model+ NR2B inhibitor group. The model of brachial plexus lower trunk avulsion injury (BPA-NP) in rats. The expression of CCL2 and its receptor CCR2 in the spinal dorsal horn of Cn 8 to Tn 1 segment were detected. Western blot was used to detect the expression of CCL2, CCR2 and NR2B in the spinal dorsal horn of Cn 8 to Tn 1 segment.n Results:Compared with BPA-NP model+ CCR2 inhibitor intervention group and blank control group, the immunofluorescence quantification and protein expression of CCL2 and CCR2 in the spinal dorsal horn of Cn 8 to Tn 1 segment of BPA-NP model+ saline group were significantly increased, which was statistically significant; the addition of CCR2, Jak and NR2B inhibitors could not completely inhibit the expression of CCL2 and CCR2, nor the expression of NR2B completely.n Conclusion:The traumatic factors can increase the expression of CCL2 in the spinal dorsal horn of Cn 8 to Tn 1 segment of BPA-NP rats, and then CCL2 can be combined with its receptor CCR2 through activating the downstream JAK/STAT signal pathway, but not the only one, which can up-regulate the expression of NMDA receptor NR2B, enhance the central sensitization and lead to the occurrence of NP. CCL2-JAK/STAT-NMDA pathway may be one of the mechanisms of NP induced by BPA.n