Cellular targets of brain inflammation in stroke.
Cellular targets of brain inflammation in stroke.
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发表时间：
2003-05
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通讯作者：
H. Han;M. Yenari
中科院分区：
文献类型：
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作者：
H. Han;M. Yenari
缺血会在受伤的大脑中引发由多种因素介导的炎症反应，导致炎症细胞积聚。反过来，这些细胞产生有毒和修复物质。炎症反应，其具有快速发作并在中风后持续，被认为是急性促成组织损伤的演变。这些信号通路的知识导致了中风治疗的各种治疗靶点的确定，特别是在再灌注阶段。这些靶点是否能用于开发治疗人类中风的疗法尚不清楚，但它们为科学研究提供了肥沃的土壤。
Ischemia elicits an inflammatory response in the injured brain that is mediated by various factors, leading to the accumulation of inflammatory cells. These cells, in turn, generate both toxic and reparative substances. The inflammatory reaction, which has a rapid onset and continues after the stroke, is thought to acutely contribute to the evolution of tissue injury. Knowledge of these signaling pathways has led to the identification of a variety of therapeutic targets for stroke treatment, particularly during the reperfusion phase. Whether these targets will be useful in the development of therapies for the treatment of stroke in humans is far from clear, but they provide fertile ground for scientific investigation.