Objective Cysteinyl leukotrienes(CysLTs)induce inflammatory responses mediated by activating CysLT1 and CysLT2 receptor.We have recently reported CysLT2 receptor is involved in neuron injury,astrocytosis and mierogliosis after focal cerebral ischemia in rats.HAMI3379 is a selective CysLT2 receptor antagonist,whether HAMI3379 can exert protective effect on focal cerebral ischemia in rats remains unknown.Under chloral hydrate anesthesia,transient focal cerebral ischemia was induced in rats by 30min of middle cerebral artery occlusion(MCAO),followed by 24h of reperfusion.PBS as vehicle,pranlukast(0.1 mg/kg,i.p.)as a positive control or HAMI3379(i.c.v.)at the doses of 1,10,100 ng was administered at 30 min before induction of ischemia.Subsequently,24h after MCAO behavior assessment,brain edema,infarct volume,neuronal damage and IgG exudation were evaluated.HAMI3379 at the doses of 10,100 ng could decrease lesion volume,brain edema,IgG exudation,neuron degeneration,and neuron loss.This protective effect was similar to CysLT1 receptor antagonist pranlukast.HAMI3379 at the dose of lng had no obvious effect on the cerebral ischemia injury.Thus,HAMI3339 has a dose-dependent neuroprotective effects on transient focal cerebral ischemia in rats,with an effective dose range of 10-100 ng.These findings further support CysLT2 receptor plays regulatory roles in acute neuron injury and the therapeutic potential of CysLT2 receptor antagonists in the treatment of cerebral ischemia at earlier phases.Future studies need to be conducted in order to determine the effects of CysLT2 receptor on the late phase of ischemic injury and the potential mechanism.