Kim J Y, Kawabori M, Yenari M A
Dept. of Neurology, University of California, San Francisco and Veterans Affairs Medical Center, San Francisco, California 4150 Clement Street, San Francisco, CA 94121, USA.
Curr Med Chem. 2014;21(18):2076-97. doi: 10.2174/0929867321666131228205146.
Stroke is a frequent cause of long-term disability and death worldwide. Ischemic stroke is more commonly encountered compared to hemorrhagic stroke, and leads to tissue death by ischemia due to occlusion of a cerebral artery. Inflammation is known to result as a result of ischemic injury, long thought to be involved in initiating the recovery and repair process. However, work over the past few decades indicates that aspects of this inflammatory response may in fact be detrimental to stroke outcome. Acutely, inflammation appears to have a detrimental effect, and anti-inflammatory treatments have been been studied as a potential therapeutic target. Chronically, reports suggest that post-ischemic inflammation is also essential for the tissue repairing and remodeling. The majority of the work in this area has centered around innate immune mechanisms, which will be the focus of this review. This review describes the different key players in neuroinflammation and their possible detrimental and protective effects in stroke. A better understanding of the roles of the different immune cells and their temporal profile of damage versus repair will help to clarify more effective modulation of inflammation post stroke.
中风是全球长期残疾和死亡的常见原因。与出血性中风相比，缺血性中风更为常见，它是由于脑动脉闭塞导致局部缺血，进而引起组织死亡。已知炎症是缺血性损伤的结果，长期以来人们认为炎症参与启动恢复和修复过程。然而，过去几十年的研究表明，这种炎症反应的某些方面实际上可能对中风预后有害。在急性期，炎症似乎具有有害作用，抗炎治疗已作为一种潜在的治疗靶点进行研究。在慢性期，有报告表明缺血后炎症对于组织修复和重塑也至关重要。该领域的大多数研究都集中在固有免疫机制上，这将是本综述的重点。本综述描述了神经炎症中不同的关键参与者及其在中风中可能产生的有害和保护作用。更好地理解不同免疫细胞的作用及其损伤与修复的时间特征，将有助于阐明中风后更有效的炎症调节方法。
