Inflammation in ischaemic brain injury: Current advances and future perspectives
Inflammation in ischaemic brain injury: Current advances and future perspectives
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DOI：
10.1111/j.1440-1681.2009.05279.x
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发表时间：
2010-02-01
影响因子：
2.9
通讯作者：
Ying, Weihai
中科院分区：
文献类型：
--
作者：
Xia, Weiliang;Han, Jin;Ying, Weihai
1.大量研究表明炎症在缺血性脑损伤中起关键作用。脑缺血再灌注引起的炎症反应包括小胶质细胞和星形胶质细胞活性增加，细胞因子、趋化因子、粘附分子和金属蛋白酶产生增加以及单核细胞和白细胞向受损脑区的浸润。2．尽管很大一部分炎症反应似乎会加剧缺血性脑损伤，但某些炎症反应对缺血性脑有益。有必要进一步识别有害和有益的炎症反应，以便为脑卒中患者设计治疗策略，选择性抑制有害反应，同时增强有益反应。3．越来越多的证据还表明，中风患者和脑缺血动物的外周免疫系统发生显着变化。值得阐明这些变化对缺血性脑损伤的影响。4．在缺血性大脑中，小胶质细胞与其他细胞类型（包括神经元、星形胶质细胞、内皮细胞和干细胞）之间存在复杂的相互作用。特别值得关注的是确定高迁移率基团 box-1、高级糖基化终产物受体 (RAGE)、S100B 和 NADPH 氧化酶在这些相互作用中的作用机制。5．由于脑缺血引起的炎症是一个相对持久的事件，对脑损伤具有深远的影响，因此进一步研究缺血性脑炎症的机制具有相当重要的意义。
1. Numerous studies have indicated that inflammation plays a key role in ischaemic brain injury. Brain ischaemia-reperfusion-induced inflammatory responses include increased microglial and astrocyte activity, increased production of cytokines, chemokines, adhesion molecules and metalloproteinases and the infiltration of monocytes and leucocytes into injured brain regions.2. Although a significant proportion of the inflammatory response appears to exacerbate ischaemic brain injury, certain inflammatory responses are beneficial to ischaemic brains. It is necessary to further identify the detrimental and beneficial inflammatory responses so that therapeutic strategies can be designed for stroke patients to selectively inhibit detrimental responses while enhancing beneficial responses.3. Increasing evidence also indicates significant changes in the peripheral immune system of stroke patients and animals that undergo cerebral ischaemia. It is worth elucidating the effects of these changes in ischaemic brain damage.4. There are complex interactions in the ischaemic brain between microglia and other cell types, including neurons, astrocytes, endothelial cells and stem cells. It is of particular interest to determine the mechanisms underlying the roles of high-mobility group box-1, advanced glycation end-products receptors (RAGE), S100B and NADPH oxidase in these interactions.5. Because brain ischaemia-induced inflammation is a relatively long-lasting event with profound effects on brain injury, it is of considerable importance to further investigate the mechanisms underlying inflammation in ischaemic brains.