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Intracerebral hemorrhage (ICH) results from blood vessels rupture in the brain, forming a blood clot in the brain parenchyma. Leakage of blood constituents causes detrimental tissue damages, ensuing long-lasting neurological deficits; however, effective therapeutic approaches are not yet developed to date. In this study, leukotriene B 4 (LTB 4 ) and its receptor leukotriene B 4 receptor 1 (BLT1) are proposed as novel therapeutic targets for ICH therapy. After the onset of ICH, the LTB 4 content in the brain transiently elevated. Microglia are considered as the source of LTB 4 production. Thrombin, a blood constituent, activated the BV-2 microglia and increased the LTB 4 secretion from the BV-2 cells. Microglia-released LTB 4 promoted its own microglial activation and neutrophil-like differentiated HL-60 cell migration activity. LTB 4 receptors comprised of two types: BLT1 and BLT2, with BLT1 known to be a high-affinity receptor associated with chemotaxis. BLT1 knockout mice showed decreased neutrophil invasion, attenuating sensorimotor dysfunction after ICH. Furthermore, therapeutic administration of ONO-4057, an orally active LTB 4 receptor antagonist, attenuated neutrophil invasion, microglial activation, axonal fragmentation, and sensorimotor deficits induced by ICH. These results suggest that LTB 4 and its receptor BLT1 can be potential promising therapeutic targets that prevent tissue damages following ICH.

A Research on Drug Discovery for Intracerebral Hemorrhage Focusing on Leukotriene B<sub>4</sub> and Its Receptor