各种内源性、外源性和系统性因素均可影响脑血流的神经血管内单位,但又互为导致血管闭塞的独立因素。无论何种机制引起的脑缺血,其结局均相同,包括血管因素、星形胶质细胞、神经元和诱发神经炎症疾病谱的周围小胶质细胞。而神经炎症反应则为缺血级联反应中的重要环节,可引起神经细胞去极化和炎性细胞因子前体激活,继而细胞死亡。神经炎症反应可引起中枢神经系统急性能量衰竭、兴奋性毒性反应、电解质紊乱、离子通道功能障碍和氧自由基分泌增多等一系列反应,而又可以是其后果。若在阈值期内缺血状态不能得到改善,则可激活基质金属蛋白酶,导致脑组织广泛损害,而即早基因激活将致使神经体液微内环境和血脑脊液屏障破坏。脱氧和复氧均可造成卒中相关性损伤。缺血性脑损伤级联反应的病理过程还包括小胶质细胞和星形胶质细胞活化,释放细胞因子、氧自由基、神经毒性因子和神经营养因子等化学介质,进一步加重脑损伤。与此同时,中性粒细胞活化并通过细胞内黏附因子结合到内皮细胞表面,然后移行至缺血核心区,加剧脑组织损伤。单核细胞和巨噬细胞通过释放炎性细胞因子和转化为吞噬细胞而在缺血性脑损伤过程中发挥作用。针对神经炎症不同环节的治疗原则,是停止或减轻脑损伤程度,如抑制细胞内黏附分子(ICAMs)、血管细胞黏附分子(VCAMs)、中性粒细胞、小胶质细胞、主要组织相容性复合物(MHC)、细胞因子、趋化因子和自由基活性。上述针对脑缺血后神经炎症的各种治疗方法,动物实验已有可喜的结果,但临床试验未见成效,目前正在做进一步研究。然而,了解神经炎症的病理学机制,对今后开发新型神经保护治疗方法的开拓脑缺血治疗领域至关重要。本文旨在阐述缺血性卒中相关神经炎症反应的不同病理学机制。 A variety of endogenous, exogenous and systemic factors can affect cerebral blood flow within the neurovascular units, but each other as an independent factor leading to vascular occlusion. Regardless of the mechanism of cerebral ischemia, the outcomes are the same, including vascular factors, astrocytes, neurons, and peripheral microglial cells that induce a spectrum of neuroinflammatory disorders. The neuroinflammatory reaction is an important link in the ischemic cascade, which can cause depolarization of nerve cells and activation of proinflammatory cytokines, leading to cell death. Neuroinflammatory reactions can cause a series of reactions, such as acute energy failure of the central nervous system, excitotoxic reactions, electrolyte imbalance, ion channel dysfunction and increased secretion of oxygen free radicals, which may be the consequence. If the ischemic state can not be improved within the threshold period, matrix metalloproteinase may be activated, resulting in extensive damage to brain tissue, whereas immediate early gene activation will result in disruption of neuro-humoral microenvironment and blood-cerebrospinal fluid barrier. Both deoxygenation and reoxygenation can cause stroke-related injuries. The pathological process of the cascade of ischemic brain injury also includes the activation of microglia and astrocytes, the release of cytokines, oxygen free radicals, neurotoxic factors and neurotrophic factors and other chemical mediators, further aggravating brain injury. In the meantime, neutrophils activate and bind to the surface of endothelial cells through intracellular adhesion molecules, then migrate to the ischemic core area and exacerbate brain injury. Monocytes and macrophages play a role in ischemic brain injury by releasing inflammatory cytokines and transforming them into phagocytes. The principles of treatment for different aspects of neuroinflammation are to stop or reduce the degree of brain injury, such as inhibition of intracellular adhesion molecules (ICAMs), vascular cell adhesion molecules (VCAMs), neutrophils, microglial cells, major histocompatibility Complex (MHC), cytokines, chemokines and free radical activity. The various treatment methods for neurological inflammation after cerebral ischemia, animal experiments have been gratifying results, but no clinical trials, is currently under further study. However, understanding the pathological mechanisms of neuroinflammation is crucial for the development of novel methods of neuroprotective treatment for the development of cerebral ischemia in the future. This article aims to elucidate the different pathological mechanisms of ischemic stroke-related neuroinflammation.