Department of Neuroscience, University of Connecticut Health Center, Farmington, Connecticut, USA.
Acta Pharmacol Sin. 2013 Sep;34(9):1121-30. doi: 10.1038/aps.2013.89. Epub 2013 Jul 29.
Inflammation plays a critical role in mediating brain injury induced by neonatal hypoxic ischemic encephalopathy (HIE). The mechanisms underlying inflammatory responses to ischemia may be shared by neonatal and adult brains; however, HIE exhibits a unique inflammation phenotype that results from the immaturity of the neonatal immune system. This review will discuss the current knowledge concerning systemic and local inflammatory responses in the acute and subacute stages of HIE. The key components of inflammation, including immune cells, adhesion molecules, cytokines, chemokines and oxidative stress, will be reviewed, and the differences between neonatal and adult inflammatory responses to cerebral ischemic injury will also be discussed.
炎症在介导新生儿缺氧缺血性脑病(HIE)引起的脑损伤中起着关键作用。导致缺血后炎症反应的机制在新生儿和成人的大脑中可能是共有的;然而,HIE 表现出一种独特的炎症表型,这是由于新生儿免疫系统的不成熟。本综述将讨论目前关于 HIE 急性期和亚急性期全身和局部炎症反应的知识。将回顾炎症的关键组成部分,包括免疫细胞、黏附分子、细胞因子、趋化因子和氧化应激,并讨论新生儿和成人对脑缺血损伤的炎症反应的差异。