Treatments with LCN2 mAb within a clinically relevant time window significantly attenuated the induction of LCN2 mRNA and protein, pro-inflammatory mediators (iNOS, IL-6, CCL2, CCL9), infiltration of neutrophils, BBB leakage, and cerebral infarction, and improved functional outcomes after stroke. The gene discussed is LCN2; the disease is brain infarction.