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创伤性脑损伤后促炎细胞因子的双重作用。

Bifunctional role of pro-inflammatory cytokines after traumatic brain injury.

作者信息

Sordillo Peter P, Sordillo Laura A, Helson Lawrence

机构信息

a SignPath Pharma, Inc. , Quakertown , PA , USA.

出版信息

Brain Inj. 2016;30(9):1043-53. doi: 10.3109/02699052.2016.1163618. Epub 2016 Jun 3.

Abstract

BACKGROUND

Pro-inflammatory cytokines play an essential role in maintenance of normal brain function as well as in repair after traumatic brain injuries (TBI). However, massive and uncontrolled release of these cytokines, particularly interleukin (IL)-1β, IL-6 and tumour necrosis factor (TNF)-α, can also result in a great deal of additional brain damage. Levels of these cytokines may increase in the brain thousands of times more than do the corresponding levels in serum.

RESEARCH DESIGN

Narrative literature review. Outcome and conclusions: Strategies to control the levels of these pro-inflammatory cytokines and to reduce the cytokine-induced brain damage are discussed. There is extensive evidence from experiments in animal models that suppression of cytokines is effective in ameliorating neurologic damage after TBI. However, the efficacy of this approach remains to be proven in patient trials.

摘要

背景

促炎细胞因子在维持正常脑功能以及创伤性脑损伤(TBI)后的修复过程中发挥着重要作用。然而,这些细胞因子的大量且不受控制的释放,尤其是白细胞介素(IL)-1β、IL-6和肿瘤坏死因子(TNF)-α,也会导致大量额外的脑损伤。这些细胞因子在脑中的水平可能比血清中的相应水平增加数千倍。

研究设计

叙述性文献综述。结果与结论:讨论了控制这些促炎细胞因子水平以及减少细胞因子诱导的脑损伤的策略。动物模型实验中有大量证据表明,抑制细胞因子对改善TBI后的神经损伤有效。然而,这种方法在患者试验中的疗效仍有待证实。

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