Rothman Sarah M, Huang Zhong, Lee Kathryn E, Weisshaar Christine L, Winkelstein Beth A
Department of Bioengineering, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6321, USA.
J Pain. 2009 Jan;10(1):90-9. doi: 10.1016/j.jpain.2008.07.008. Epub 2008 Oct 10.
Inflammatory cytokines contribute to lumbar radiculopathy. Regulation of cytokines for transient cervical injuries, with or without longer-lasting inflammation, remains to be defined. The C7 root in the rat underwent compression (10gf), chromic gut suture exposure (chr), or their combination (10gf+chr). Ipsilateral C7 spinal cord and dorsal root ganglia (DRG) were harvested at 1 hour after injury for real-time PCR analysis of IL-1beta, IL-6, and TNF-alpha. Cytokine mRNA increased after all 3 injuries. TNF-alpha mRNA in the DRG was significantly increased over sham after 10gf+chr (P = .026). Spinal IL-1beta was significantly increased over sham after 10gf and 10gf+chr (P < .024); IL-6 was significantly increased after 10gf+chr (P < .024). In separate studies, the soluble TNF-alpha receptor was administered at injury and again at 6 hours in all injury paradigms. Allodynia was assessed and tissue samples were harvested for cytokine PCR. Allodynia significantly decreased with receptor administration for 10gf and 10gf+chr (P < .005). Treatment also significantly decreased IL-1beta and TNF-alpha mRNA in the DRG for 10gf+chr (P < .028) at day 1. Results indicate an acute, robust cytokine response in cervical nerve root injury with varying patterns, dependent on injury type, and that early increases in TNF-alpha mRNA in the DRG may drive pain-related signaling for transient cervical injuries.
Inflammatory cytokine mRNA in the DRG and spinal cord are defined after painful cervical nerve root injury. Studies describe a role for TNF-alpha in mediating behavioral sensitivity and inflammatory cytokines in transient painful radiculopathy. Results outline an early response of inflammatory cytokine upregulation in cervical pain.
炎性细胞因子与腰椎神经根病有关。对于伴有或不伴有持续性炎症的短暂性颈部损伤,细胞因子的调节作用尚待明确。对大鼠的C7神经根进行压迫(10克力)、铬肠线缝合暴露(chr)或两者联合(10克力+chr)。在损伤后1小时采集同侧C7脊髓和背根神经节(DRG),用于实时PCR分析白细胞介素-1β、白细胞介素-6和肿瘤坏死因子-α。三种损伤后细胞因子mRNA均增加。在10克力+chr后,DRG中的肿瘤坏死因子-α mRNA比假手术组显著增加(P = 0.026)。在10克力和10克力+chr后,脊髓白细胞介素-1β比假手术组显著增加(P < 0.024);在10克力+chr后,白细胞介素-6显著增加(P < 0.024)。在单独的研究中,在所有损伤模型中,于损伤时及损伤后6小时给予可溶性肿瘤坏死因子-α受体。评估痛觉过敏情况,并采集组织样本进行细胞因子PCR检测。给予受体后,10克力和10克力+chr组的痛觉过敏显著减轻(P < 0.005)。在第1天,治疗还显著降低了10克力+chr组DRG中白细胞介素-1β和肿瘤坏死因子-α mRNA的水平(P < 0.028)。结果表明,在颈部神经根损伤中存在急性、强烈的细胞因子反应,其模式各异,取决于损伤类型,并且DRG中肿瘤坏死因子-α mRNA的早期增加可能驱动短暂性颈部损伤的疼痛相关信号传导。
在疼痛性颈部神经根损伤后,明确了DRG和脊髓中的炎性细胞因子mRNA。研究描述了肿瘤坏死因子-α在介导行为敏感性方面的作用以及炎性细胞因子在短暂性疼痛性神经根病中的作用。结果概述了颈部疼痛中炎性细胞因子上调的早期反应。