Involvement of cytokine network in the pathology of neuropathic pain following peripheral nerve injury

肿瘤坏死因子-α是一种促炎性细胞因子，可能在神经损伤后神经病理性疼痛的诱导中起关键作用。然而，神经损伤后脊髓组织中肿瘤坏死因子α及其受体mRNA的精确组织学表达尚不完全清楚。SNI后18h出现一过性升高，伤后2 4h达高峰。在幼年大鼠脊髓中，肿瘤坏死因子α和肿瘤坏死因子受体2低水平表达，在背角神经元和神经胶质细胞中检测到肿瘤坏死因子受体1的mRNA信号。SNI后24小时，同侧小胶质细胞内的肿瘤坏死因子-αm RNA信号增强。SNI后3d，同侧神经胶质细胞内TNFR1和TNFR2的mRNA信号明显增强。

Tumor necrosis factor(TNF)-alpha is one of a pro-inflammatory cytokines that may play a key role for the induction of neuropathic pain following nerve injury. However, the precise histological expression of TNF alpha and its receptors mRNA in the spinal cord after nerve injury is not fully understood. TNF alpha mRNA showed the transient increase from 18 hour and peaked at 24 hour following SNI. In the spinal cord of naive rats, TNF alpha and TNFR2 showed a low level expression and TNFR1 mRNA signal was detected in neurons and glial cells in the dorsal horn. Twenty-four hours after SNI, TNF alpha mRNA signals increased in the ipsilateral microglia. TNFR1 and TNF R2 mRNA signals increased strikingly in ipsilateral glial cells at 3 days after SNI.