脂质运载蛋白-2与缺血性卒中

Lipocalin-2 and ischemic stroke

炎症在缺血性卒中的病理生理学过程中起重要作用。实验研究显示,星形胶质细胞产生的脂质运载蛋白-2(lipocalin-2, LCN2)参与了缺血性卒中后的炎症机制,并加重缺血性脑损伤。临床研究显示,缺血性卒中患者外周血LCN2增高与转归不良以及死亡风险相关。需要进一步研究揭示LCN2在脑缺血再灌注损伤中的具体机制,特别是LCN2介导的信号通路,并寻找靶向LCN2的可能治疗方法。

Inflammation plays an important role in the pathophysiological process of ischemic stroke.Experimental results have shown that the lipocalin-2(LCN2)produced by astrocytes is involved in the inflammatory mechanism of ischemic stroke and aggravates the ischemic brain damage.Clinical studies have shown that the increased LCN2 in peripheral blood of patients with ischemic stroke is associated with the poor outcomes and risk of death.Further research is needed to reveal the specific mechanism of LCN2 in cerebral ischemia-reperfusion injury,especially the signaling pathway mediated by LCN2,and look for possible treatments targeting LCN2.