Preclinical and clinical research on inflammation after intracerebral hemorrhage.
Preclinical and clinical research on inflammation after intracerebral hemorrhage.
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DOI：
10.1016/j.pneurobio.2010.08.001
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发表时间：
2010-12
影响因子：
6.7
通讯作者：
Wang, Jian
中科院分区：
文献类型：
--
作者：
Wang, Jian
关键词：
脑出血(ICH)是致命性最高的卒中亚型之一。尽管与脑出血相关的发病率和死亡率很高，但其病理生理机制还没有像缺血性中风那样被研究。来自临床前和临床研究的现有证据表明，炎症机制参与了脑出血继发性脑损伤的进展。例如，在临床前脑出血模型中，小胶质细胞的激活已被证明在1小时内发生，远远早于中性粒细胞的渗透。最近我们对神经炎性通路的了解进展揭示了几个新的分子靶点，相关的治疗策略已经在临床前脑出血模型中进行了测试。本文综述了近年来脑出血临床前模型的研究进展，综述了炎症细胞(白细胞、巨噬细胞、小胶质细胞和星形胶质细胞)和炎症介质(基质金属蛋白酶、核因子红系相关因子2、血红素加氧酶和铁)的临床前和临床研究，并重点介绍了新兴的治疗领域。
Intracerebral hemorrhage (ICH) is one of the most lethal stroke subtypes. Despite the high morbidity and mortality associated with ICH, its pathophysiology has not been investigated as well as that of ischemic stroke. Available evidence from preclinical and clinical studies suggests that inflammatory mechanisms are involved in the progression of ICH-induced secondary brain injury. For example, in preclinical ICH models, microglial activation has been shown to occur within 1 h, much earlier than neutrophil infiltration. Recent advances in our understanding of neuroinflammatory pathways have revealed several new molecular targets, and related therapeutic strategies have been tested in preclinical ICH models. This review summarizes recent progress made in preclinical models of ICH, surveys preclinical and clinical studies of inflammatory cells (leukocytes, macrophages, microglia, and astrocytes) and inflammatory mediators (matrix metalloproteinases, nuclear factor erythroid 2-related factor 2, heme oxygenase, and iron), and highlights the emerging areas of therapeutic promise.
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