Laboratory of Ischemic and Neurodegenerative Brain Research, Mossakowski Medical Research Institute, Polish Academy of Sciences, PL 02-106 Warsaw, Poland.
Department of Pathophysiology, Medical University of Lublin, PL 20-090 Lublin, Poland.
Int J Mol Sci. 2021 Apr 23;22(9):4405. doi: 10.3390/ijms22094405.
One of the leading causes of neurological mortality, disability, and dementia worldwide is cerebral ischemia. Among the many pathological phenomena, the immune system plays an important role in the development of post-ischemic degeneration of the brain, leading to the development of neuroinflammatory changes in the brain. After cerebral ischemia, the developing neuroinflammation causes additional damage to the brain cells, but on the other hand it also plays a beneficial role in repair activities. Inflammatory mediators are sources of signals that stimulate cells in the brain and promote penetration, e.g., T lymphocytes, monocytes, platelets, macrophages, leukocytes, and neutrophils from systemic circulation to the brain ischemic area, and this phenomenon contributes to further irreversible ischemic brain damage. In this review, we focus on the issues related to the neuroinflammation that occurs in the brain tissue after ischemia, with particular emphasis on ischemic stroke and its potential treatment strategies.
脑缺血是全球导致神经死亡、残疾和痴呆的主要原因之一。在众多病理现象中，免疫系统在脑缺血后退行性变的发展中起着重要作用，导致脑内神经炎症发生变化。脑缺血后，发展中的神经炎症会对脑细胞造成额外的损伤，但另一方面它也对修复活动起到有益的作用。炎症介质是刺激大脑细胞并促进穿透的信号源，例如 T 淋巴细胞、单核细胞、血小板、巨噬细胞、白细胞和中性粒细胞从全身循环进入脑缺血区，这一现象导致进一步的不可逆转的缺血性脑损伤。在这篇综述中，我们重点关注与缺血后脑组织中发生的神经炎症相关的问题，特别强调了缺血性脑卒中及其潜在的治疗策略。
