Liu Chenglong, Zhang Fei, Liu Haihua, Wei Fang
MD, Associate chief Physician, Department of Anaesthesiology, Gaoyou People's Hospital, Gaoyou Hospital Affiliated, Soochow University, China. Conception and design of the study, manuscript preparation, final approval.
MD, Physician, Department of Anaesthesiology, Gaoyou People's Hospital, Gaoyou Hospital Affiliated, Soochow University, China. Acquisition, analysis and interpretation of data; manuscript preparation.
Acta Cir Bras. 2018 Jul;33(7):619-628. doi: 10.1590/s0102-865020180070000007.
To evaluate the role of CX3CL1 and NF-κB in the lumbar disc herniation induced neuropathic pain.
After LDH induced by implantation of autologous nucleus pulposus (NP) on the left L5 nerve root was established, mechanical thresholds and thermal hyperalgesia were tested at relevant time points during an observation period of 28 days. Expression of CX3CL1 and NF-κBin the dorsal root ganglion (DRG) were performed by using Western blotting and RT-PCR.
Implantation of autologous nucleus pulposus (NP) induced neuropathic pain, associated with increased mRNA and protein expression of CX3CL1 in the DRG. Moreover, intrathecal injection of neutralizing antibody against CX3CL1 could attenuates LDH-induced persistent pain hypersensitivity. Interestingly, NF-κB activation in the DRGs were found in LDH-induced neuropathic pain. Furthermore, NF-κB downregulation by p65 inhibitor PDTC markedly alleviated LDH-induced mechanical allodynia and thermal hyperalgesia in rat. Importantly, CX3CL1 neutralizing antibody (10 μg/10 μl, i.t.) reduces p-p65 protein level in DRG.
CX3XL1 could regulate LDH-induced neuropathic pain through NF-κB pathway. Targeting CX3CL1 and NF-κB may represent a potential treatment for neuropathic pain caused by LDH.
评估CX3CL1和核因子κB（NF-κB）在腰椎间盘突出症所致神经性疼痛中的作用。
通过在左侧L5神经根植入自体髓核建立腰椎间盘突出症（LDH）模型后，在28天的观察期内的相关时间点测试机械阈值和热痛觉过敏。采用蛋白质免疫印迹法和逆转录-聚合酶链反应（RT-PCR）检测背根神经节（DRG）中CX3CL1和NF-κB的表达。
自体髓核植入诱发神经性疼痛，伴有DRG中CX3CL1的mRNA和蛋白表达增加。此外，鞘内注射抗CX3CL1中和抗体可减轻LDH诱发的持续性疼痛超敏反应。有趣的是，在LDH诱发的神经性疼痛中发现DRG中有NF-κB激活。此外，p65抑制剂吡咯烷二硫代氨基甲酸盐（PDTC）下调NF-κB可明显减轻大鼠LDH诱发的机械性异常疼痛和热痛觉过敏。重要的是，CX3CL1中和抗体（10μg/10μl，鞘内注射）可降低DRG中磷酸化p65蛋白水平。
CX3CL1可通过NF-κB途径调节LDH诱发的神经性疼痛。靶向CX3CL1和NF-κB可能是治疗LDH所致神经性疼痛的一种潜在方法。
