Intracerebral hemorrhage (ICH) results from the rupture of blood vessels and the leakage of blood constituents. Especially, thrombin, a blood coagulation factor, activates microglia and promotes ICH pathology. Furthermore, neutrophils infiltrated by blood leakage also exacerbates the ICH. Our previous study showed that leukotriene B₄ (LTB₄), a bioactive lipid, promotes pathological progression of ICH (Hijioka et al., 2017). In this study, we focused on lipoxin A₄ (LXA₄), other bioactive lipid synthesized by the enzymes producing LTB₄. Thrombin (30 U/mL) treatment for 12 h increased mRNA expression of inducible nitric oxide synthase (iNOS) in BV-2 microglia. Then, differentiated human promyelocytic leukemia cells (dHL-60) induced by dimethyl sulfoxide were seeded on upper layer of cell culture inserts with 3.0 μm pore, and treated culture supernatant of BV-2 cells with 12 h thrombin treatment to bottom layer. Culture supernatant of thrombin-treated BV-2 cells promotes infiltration of dHL-60 cells into the bottom layer, but LXA₄ treatment suppressed the infiltration. These results suggest that mediators secreted by microglia promote neutrophils invasion and LXA₄ can be suppress the neutrophils invasion followed to ICH.