Pranlukast reduces neutrophil but not macrophage/microglial accumulation in brain after focal cerebral ischemia in mice
Abstract
Aim: To determine whether pranlukast, a cysteinyl leukotriene receptor-1 antagonist, exerts an anti-inflammatory effect on focal cerebral ischemia in mice.
Methods: Focal cerebral ischemia in mice was induced by permanent middle cerebral artery occlusion (MCAO). In addition to neurological deficits, infarct volume, degenerated neurons and endogenous IgG exudation, we detected accumulation of neutrophils and macrophage/microglia in the ischemic brain tissue 72 h after MCAO. Pranlukast was ip injected 30 min before and after MCAO.
Results: Pranlukast significantly attenuated neurological deficits, infarct volume, neuron degeneration and IgG exudation. Importantly, pranlukast (0.01 and 0.1 mg/kg) inhibited myeloperoxidase-positive neutrophil, but not CD 11b-positive macrophage/microglial accumulation in the ischemic cortical tissue.
Conclusion: Pranlukast exerts an anti-inflammatory effect on focal cerebral ischemia in the subacute phase that is limited to neutrophil recruitment through the disrupted blood-brain barrier.
Keywords:
Methods: Focal cerebral ischemia in mice was induced by permanent middle cerebral artery occlusion (MCAO). In addition to neurological deficits, infarct volume, degenerated neurons and endogenous IgG exudation, we detected accumulation of neutrophils and macrophage/microglia in the ischemic brain tissue 72 h after MCAO. Pranlukast was ip injected 30 min before and after MCAO.
Results: Pranlukast significantly attenuated neurological deficits, infarct volume, neuron degeneration and IgG exudation. Importantly, pranlukast (0.01 and 0.1 mg/kg) inhibited myeloperoxidase-positive neutrophil, but not CD 11b-positive macrophage/microglial accumulation in the ischemic cortical tissue.
Conclusion: Pranlukast exerts an anti-inflammatory effect on focal cerebral ischemia in the subacute phase that is limited to neutrophil recruitment through the disrupted blood-brain barrier.