脊髓继发性损伤后细胞因子的表达及其对细胞凋亡的作用
王诗军1
李钰婷2
李淳德1
1.100034,北京大学第一医院骨科2.100034,北京大学第一医院麻醉科
摘要：Secondary spinal cord injuries are associated with inflammation, excessive cytokine release, and cell apoptosis. Apoptosis is known as the main mode of delayed neuronal cell death after spinal cord injury and is mediated by a variety of pro-inflammatory cytokines. Cytokines are important regulatory molecules that are involved in the regulation of immune and inflammatory response and cell apoptosis after spinal cord injury. Interleukin-1 ( IL-1 ), interleukin-6 ( IL-6 ), interleukin-8 ( IL-8 ) and tumor necrosis factor alpha ( TNF-α ) play an important role in spinal cord injury. IL-1β can lead to protein degradation and then induce cell apoptosis, the expression of IL-1β is increased after spinal cord injury, a peak of IL-1β expression is observed within 6h. The expression of TNF-α is increased after spinal cord injury which induce apoptosis in neurons and oligodendrocytes. A peak TNF-α expression is observed within 1 h after spinal cord injury, and TUNEL-positive cells are observed. After injection with TNF-α antagonist into the injured area, the expression of iNOS and the level of NO are decreased, and the number of TUNEL-positive cell are reduced. Inhibition of pro-inflammatory cytokines expression can reduce cell apoptosis and inflammatory responses in cells, that play a neuroprotective role in promoting neural repair and regeneration after spinal cord injury.
关键词：脊髓损伤继发性细胞凋亡细胞因子类神经元白细胞介素类
论文发表日期：2016-01-01
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：6( 432-437 )
英文信息