Frontiers in Research Review: Stroke Inflammation in ischaemic brain injury: Current advances and future perspectives
Frontiers in Research Review: Stroke Inflammation in ischaemic brain injury: Current advances and future perspectives
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发表时间：
2010
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通讯作者：
W. Xia;Jin Han;Gang Huang;andWeihai Ying
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作者：
W. Xia;Jin Han;Gang Huang;andWeihai Ying
1.大量研究表明，炎症在缺血性脑损伤中起着关键作用。脑缺血-再灌注诱导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的产生增加，以及单核细胞和白细胞向受损脑区域的浸润。2.虽然很大比例的炎症反应似乎会加重缺血性脑损伤，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，以便为中风患者设计治疗策略，以选择性地抑制有害反应，同时增强有益反应。3.越来越多的证据也表明中风患者和经历脑缺血的动物的外周免疫系统发生了显着变化。这些变化对缺血性脑损伤的影响值得阐明。4.在缺血性脑中，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。特别感兴趣的是确定高迁移率族蛋白-1，晚期糖基化终产物受体（AGEs），S100 B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，对脑损伤有深远的影响，因此进一步研究缺血性脑炎症的潜在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.