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Aim: To determine whether pranlukast, a cysteinyl leukotriene receptor-lantagonist, exerts an anti-inflammatory effect on focal cerebral ischemia in mice.Methods: Focal cerebral ischemia in mice was induced by permanent middle cere-bral artery occlusion(MCAO). In addition to neurological deficits, infarct volume,degenerated neurons and endogenous IgG exudation, we detected accumulationof neutrophils and macrophage/microglia in the ischemic brain tissue 72 h afterMCAO. Pranlukast was ip injected 30 min before and after MCAO. Results:Pranlukast significantly attenuated neurological deficits, infarct volume, neurondegeneration and IgG exudation. Importantly, pranlukast(0.01 and 0.1 mg/kg)inhibited myeloperoxidase-positive neutrophil, but not CD11b-positive macroph-age/microglial accumulation in the ischemic cortical tissue. Conclusion: Pranlukastexerts an anti-inflammatory effect on focal cerebral ischemia in the subacute phasethat is limited to neutrophil recruitment through the disrupted blood-brain barrier.
Aim: To determine whether pranlukast, a cysteinyl leukotriene receptor-lantagonist, exerts an anti-inflammatory effect on focal cerebral ischemia in mice. Methods: Focal cerebral ischemia in mice was induced by permanent middle cerebal-bral artery occlusion (MCAO). 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, Importantly, pranlukast (0.01 and 0.1 mg / kg) inhibited myeloperoxidase-positive neutrophil, but not CD11b-positive macroph-age / microglial accumulation in the ischemic cortical tissue. Conclusion: Pranlukastexerts an anti-inflammatory effect on focal cerebral ischemia in the subacute phasethat is limited to neutrophil recruitment through the disrupte d blood-brain barrier.