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Cytokine mRNA expression in painful radiculopathy.

机译:神经根痛中细胞因子mRNA的表达

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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. PERSPECTIVE: 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.
机译:炎性细胞因子促成腰神经根病。对于短暂的宫颈损伤,伴或不伴持续较长时间的炎症,细胞因子的调节仍有待确定。大鼠的C7根受到压缩(10gf),铬肠缝合线暴露(chr)或其组合(10gf + chr)。损伤后1小时收集同侧C7脊髓和背根神经节(DRG),用于实时PCR分析IL-1beta,IL-6和TNF-alpha。所有3次损伤后细胞因子mRNA均升高。 10gf + chr后,DRG中的TNF-αmRNA显着高于假手术(P = .026)。脊髓IL-1β在10gf和10gf + chr后比假手术显着增加(P <.024); 10gf + chr后IL-6显着增加(P <.024)。在单独的研究中,可溶性TNF-α受体在所有损伤范例中分别在受伤时和6小时后再次给药。评估异常性疼痛并收获组织样品用于细胞因子PCR。服用10gf和10gf + chr的受体后,异常性疼痛明显减少(P <.005)。在第1天,治疗还显着降低了10gf + chr的DRG中IL-1beta和TNF-αmRNA的表达(P <.028)。结果表明,在颈神经根损伤中,不同类型的急性,强烈的细胞因子反应取决于损伤类型,并且DRG中TNF-αmRNA的早期增加可能驱动短暂性颈椎损伤的疼痛相关信号传导。透视:颈神经根痛后,DRG和脊髓中的炎性细胞因子mRNA被确定。研究描述了TNF-α在短暂性神经根痛中介导的行为敏感性和炎性细胞因子的作用。结果概述了宫颈疼痛中炎性细胞因子上调的早期反应。

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