Inflammatory responses in brain ischemia.
Inflammatory responses in brain ischemia.
复制标题
脑缺血的炎症反应。
DOI：
10.2174/0929867322666150209154036
复制
发表时间：
2015
影响因子：
4.1
通讯作者：
Yenari MA
中科院分区：
文献类型：
--
作者：
Kawabori M;Yenari MA
脑梗塞由于脑血管闭塞而引起缺血，导致组织死亡，最近的研究表明，中风后炎症对缺血性病理学的发展有显着影响。由于与动脉闭塞后原发性损伤的挽救相比，脑部炎症引起的继发性损伤可能具有更长的治疗时间窗口，因此控制炎症将是一个明显的治疗目标。近年来，该领域取得了大量的实验进展。然而，很难阐明缺血性中风后炎症反应的精确机制，因为炎症是炎症细胞和分子之间一系列复杂的相互作用，所有这些相互作用可能是有害的，也可能是有益的。我们回顾了脑缺血中神经炎症和炎症信号通路调节的最新进展。还将涵盖治疗缺血性中风的潜在目标。免疫系统和脑损伤与修复的作用将有助于阐明免疫调节如何治疗中风。
Brain infarction causes tissue death by ischemia due to occlusion of the cerebral vessels and recent work has shown that post stroke inflammation contributes significantly to the development of ischemic pathology. Because secondary damage by brain inflammation may have a longer therapeutic time window compared to the rescue of primary damage following arterial occlusion, controlling inflammation would be an obvious therapeutic target. A substantial amount of experimentall progress in this area has been made in recent years. However, it is difficult to elucidate the precise mechanisms of the inflammatory responses following ischemic stroke because inflammation is a complex series of interactions between inflammatory cells and molecules, all of which could be either detrimental or beneficial. We review recent advances in neuroinflammation and the modulation of inflammatory signaling pathways in brain ischemia. Potential targets for treatment of ischemic stroke will also be covered. The roles of the immune system and brain damage versus repair will help to clarify how immune modulation may treat stroke.