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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Early neuronal expression of tumor necrosis factor-alpha after experimental brain injury contributes to neurological impairment.
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Early neuronal expression of tumor necrosis factor-alpha after experimental brain injury contributes to neurological impairment.

机译：实验性脑损伤后，肿瘤坏死因子-α的早期神经元表达导致神经功能受损。

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摘要

Tumor necrosis factor-alpha (TNF alpha) is a pleiotropic cytokine involved in inflammatory cascades associated with CNS injury. To examine the role of TNF alpha in the acute pathophysiology of traumatic brain injury (TBI), we studied its expression, localization and modulation in a clinically relevant rat model of non-penetrating head trauma. TNF alpha levels increased significantly in the injured cortex at 1 and 4, but not at 12, 24 or 72 h after severe lateral fluid-percussion trauma (2.6-2.7 atm). TNF alpha was not elevated after mild injury. At 1 and 4 h after severe TBI, marked increases of TNF alpha were localized immunocytochemically to neurons of the injured cerebral cortex. A small population of astrocytes, ventricular cells and microvessels, also showed positive TNF alpha staining, but this expression was not injury-dependent. Macrophages that were present in a hemorrhagic zone along the external capsule, corpus callosum and alveus hippocampus at 4 h after TBI did not express TNF alpha. Intracerebroventricular administration of a selective TNF alpha antagonist--soluble TNF alpha receptor fusion protein (sTNFR:Fc) (37.5 microg)--at 15 min before and 1 h after TBI, improved performance in a series of standardized motor tasks after injury. In contrast, intravenous administration of sTNFR:Fc (0.2, 1 or 5 mg/kg) at 15 min after trauma did not improve motor outcome. Collectively, this evidence suggests that enhanced early neuronal expression of TNF alpha after TBI contributes to subsequent neurological dysfunction.
机译：肿瘤坏死因子-α（TNF alpha）是参与与CNS损伤相关的炎症级联反应的多效性细胞因子。为了检查TNFα在颅脑外伤（TBI）的急性病理生理中的作用，我们研究了其在非穿透性颅脑外伤的临床相关大鼠模型中的表达，定位和调节。严重的侧面液体撞击创伤（2.6-2.7 atm）后，受伤皮层中的TNFα水平在1和4时显着增加，但在12、24或72 h时没有升高。轻度损伤后，TNFα并未升高。严重的TBI后1和4小时，TNFα的明显增加在免疫细胞化学上定位于受伤的大脑皮层的神经元。少量的星形胶质细胞，心室细胞和微血管也显示出阳性的TNFα染色，但这种表达不是损伤依赖性的。 TBI后4小时，沿外囊，call体和海马海泡的出血区存在的巨噬细胞不表达TNFα。在TBI之前和之后1小时和之后1小时，对选择性TNFα拮抗剂-可溶性TNFα受体融合蛋白（sTNFR：Fc）（37.5 microg）进行脑室内给药可改善损伤后一系列标准化运动任务的表现。相反，创伤后15分钟静脉给予sTNFR：Fc（0.2、1或5 mg / kg）不能改善运动结局。总的来说，该证据表明，TBI后TNFα早期神经元表达的增强导致随后的神经功能障碍。

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