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

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

作     者:Li-sheng CHU~(2,3) Er-qing WEI~(2,4) Guo-liang YU~2 San-hua FANG~2 Yu ZHOU~2 Meng-ling WANG~2 Wei-ping ZHANG~2 ~2Department of Pharmacology,School of Medicine Zhejiang University.Hangzhou 310031.China:~3Department of Physiology.Zhejiang College of Traditional Chinese Medicine.Hangzhou 310053,China 

作者机构:Department of Pharmacology School of Medicine Zhejiang University Hangzhou China Department of Physiology Zhejiang College of Traditional Chinese Medicine Hangzhou China 

出 版 物:《Acta Pharmacologica Sinica》 (中国药理学报(英文版))

年 卷 期:2006年第27卷第3期

页      面:282-288页

核心收录:

学科分类:1007[医学-药学(可授医学、理学学位)] 1006[医学-中西医结合] 100706[医学-药理学] 1002[医学-临床医学] 100602[医学-中西医结合临床] 10[医学] 

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

主  题:leukotriene receptor antagonist pranlukast cerebral ischemia neuroprotection inflammation 

摘      要:Aim: To determine whether pranlukast, a cysteinyl leukotriene receptor-lantagonist, exerts an anti-inflammatory effect on focal cerebral ischemia in ***: 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.

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