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.