Department of Pharmaceutical Chemistry and Drug Analysis, Research Group Experimental Neuropharmacology, Vrije Universiteit Brussel, Laarbeeklaan 103, 1090 Brussels, Belgium.
J Neuroinflammation. 2010 Nov 1;7:74. doi: 10.1186/1742-2094-7-74.
Neuroinflammation is a key element in the ischemic cascade after cerebral ischemia that results in cell damage and death in the subacute phase. However, anti-inflammatory drugs do not improve outcome in clinical settings suggesting that the neuroinflammatory response after an ischemic stroke is not entirely detrimental. This review describes the different key players in neuroinflammation and their possible detrimental and protective effects in stroke. Because of its inhibitory influence on several pathways of the ischemic cascade, hypothermia has been introduced as a promising neuroprotective strategy. This review also discusses the influence of hypothermia on the neuroinflammatory response. We conclude that hypothermia exerts both stimulating and inhibiting effects on different aspects of neuroinflammation and hypothesize that these effects are key to neuroprotection.
神经炎症是脑缺血后缺血级联反应的一个关键因素，导致亚急性期的细胞损伤和死亡。然而，抗炎药物并没有改善临床效果，这表明缺血性中风后的神经炎症反应并非完全有害。本综述描述了神经炎症中的不同关键因素及其在中风中的潜在有害和保护作用。由于其对缺血级联反应的几个途径的抑制作用，低温已被引入作为一种有前途的神经保护策略。本综述还讨论了低温对神经炎症反应的影响。我们得出结论，低温对神经炎症的不同方面既有刺激作用，也有抑制作用，并假设这些作用是神经保护的关键。
