Pranlukast reduces neutrophil but not macrophage/microglial accumu-lation in brain after focal cerebral ischemia in mice  

作　　者：Li-sheng CHU Er-qing WEI Guo-liang YU San-hua FANG Yu ZHOU Meng-ling WANG Wei-ping ZHANG 

机构地区：[1]Department of Pharmacology, School of Medicine, Zhejiang University, Hangzhou 310031, China [2]Department of Physiology, ZhejiangCollege of Traditional Chinese Medicine, Hangzhou 310053, China

出　　处：《Acta Pharmacologica Sinica》2006年第3期282-288,共7页中国药理学报（英文版）

基　　金：Project supported by the National Natural Science Foundation of China(№30271498).

摘　　要：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 CD1 l b-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.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 CD1 l b-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.

关 键 词：leukotriene receptor antagonist PRANLUKAST cerebral ischemia NEUROPROTECTION inflammation 

分 类 号：R74[医药卫生—神经病学与精神病学]