Role of Perinatal Inflammation in Cerebral Palsy
Role of Perinatal Inflammation in Cerebral Palsy
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DOI：
10.1016/j.pediatrneurol.2008.09.016
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发表时间：
2009-03-01
影响因子：
3.8
通讯作者：
Sebire, Guillaume
中科院分区：
文献类型：
--
作者：
Girard, Sylvie;Kadhim, Hazim;Sebire, Guillaume
炎症分子在胎儿环境中和出生后脑损伤受试者中迅速上调。宫内感染和炎症常与窒息有关。因此，这种由感染或炎症和缺氧联合引起的双重打击效应是新生儿脑损伤的常见伴随物。最近设计了缺氧和感染相结合的动物模型，以探索在这种情况下脑损伤的潜在机制，并寻找可能的神经保护策略。促炎细胞因子被认为是围产期窒息、细菌感染或两者兼而有之的新生儿脑损伤的主要介质。然而，细胞因子也可能具有神经保护特性。细胞因子的神经损伤和神经保护作用之间的平衡的关键点尚未解开。这种理解可能有助于开发新的治疗方法，以抵消与脑损伤相关的病理生理机制中观察到的炎症不平衡。(C)2009年，Elsevier Inc. All rights reserved.
Inflammatory molecules are promptly upregulated in the fetal environment and postnatally in brain-damaged subjects. Intrauterine infections and inflammation are often associated with asphyxia. This double-hit effect by combined infection or inflammation and hypoxia is therefore a frequent concomitant in neonatal brain damage. Animal models combining hypoxia and infection were recently designed to explore the mechanisms underlying brain damage in such circumstances and to look for possible neuroprotective strategies. Proinflammatory cytokines are thought to be major mediators in brain injury in neonates with perinatal asphyxia, bacterial infection, or both. Cytokines, however, could also have neuroprotective properties. The critical point in the balance between neurodamaging and neuroprotective effects of cytokines has yet to be unraveled. This understanding might help to develop new therapeutic approaches to counteract the inflammatory disequilibrium observed in the pathophysiologic mechanisms associated with brain injury. (C) 2009 by Elsevier Inc. All rights reserved.