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机构地区:[1]北京大学第一医院骨科,100034 [2]北京大学第一医院麻醉科,100034
出 处:《中国骨与关节杂志》2016年第6期432-437,共6页Chinese Journal of Bone and Joint
摘 要:脊髓损伤是骨科损伤中非常常见的中枢神经系统损伤,且发生率高、致残率高。脊髓损伤可分为原发性脊髓损伤与继发性脊髓损伤。脊髓继发性损伤是在原发性损伤的基础上,在细胞分子水平上主动调节的过程,是组织发生变性坏死的过程。脊髓继发性损伤包括了局部缺血缺氧、免疫炎性反应、自由基损伤及脂质过氧化等一系列病理过程,而免疫炎性反应是继发性损伤中最为重要的病理过程之一。Secondary spinal cord injuries are associated with infl ammation, 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-infl ammatory cytokines. Cytokines are important regulatory molecules that are involved in the regulation of immune and infl ammatory 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 i NOS and the level of NO are decreased, and the number of TUNEL-positive cell are reduced. Inhibition of pro-infl ammatory cytokines expression can reduce cell apoptosis and infl ammatory responses in cells, that play a neuroprotective role in promoting neural repair and regeneration after spinal cord injury.
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