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Acta Pharmacologica Sinica 2006年第3期27卷 282-288页

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 Department of Pharmacology School of Medicine Zhejiang University Hangzhou China Department of Physiology Zhejiang College of Traditional Chinese Medicine Hangzhou China

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.

关键词： leukotriene receptor antagonist pranlukast cerebral ischemia neuroprotection inflammation

pranlukast dose-and time-dependently protects against ischemic neuronal damage in the rat hippocampus

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Pranlukast dose-and time-dependently protects against ischem...

pranlukast reduces neuronal death in the hippocampal CA1 sector induced by four- vessel occlusion in rats

两岸三地药理学与临床药理学术会议

作者： ZHANG Li-hui~1 ZHAO Jian-bo~1 YUAN Hui-ning~1 HU Quan~1 WEI Er-qing~2 (1. Department of Pharmacology, Hangzhou Normal University, Hangzhou 310036, China 2. Department of Pharmacology, Zhejiang University, Hangzhou 310058, China)

Objective Our previous studies showed that the neuroprotective effect of pranlukast,a cysteinyl leukotriene receptor-1(CysLT1)antagonist,on global cerebral ischemia in *** study was performed to evaluate dose-and time-dependent properties of pranlukast on CA1 neuron loss following transient global ischemia in *** Brain injury was induced by an improved four-vessel occlusion(4-VO)in rats. pranlukast(0.03-0.30 mg·kg)was injected intraperitoneally either as multiple doses(before or after ischemia)or as a single dose(30 min before ischemia),*** variables were monitored and neuron count was measured by computer-assisted *** The 4-VO model produced continu- ing postischemic neuronal death in CA1 *** of pranlukast(0.1 and 0.3 mg·kg,30 rain before ischemia and 1,24,48 and 72 h after ischemia)markedly reduced CA1 *** with a single dose of pranlukast(0.1mg·kg,30 min before ischemia)also resulted in a significant increase in the number of healthy CA1 neurons at 3 *** interest is the finding that pranlukast(0.1mg·kgres- cued CA1 neurons from ischemic death even when treatment was delayed until 30 min or 1 h after ischemia. Conclusions The present study confirms pranlukast has a dose-and time-dependent cerebroprotective effects on CA1 neuron loss following transient global ischemia in rats,with an effective dose range of 0.1-0.3 mg·kgand a therapeutic window of *** findings further support the therapeutic potential of CysLT1 receptor antagonists in the treatment of global cerebral ischemia.

关键词： pranlukast brain ischemia hippocampus neuroprotection

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Pranlukast reduces neuronal death in the hippocampal CA1 sec...

pranlukast dose-and time-dependently protects against ischemic neuronal damage in the rat hippocampus

中国药理学会第十次全国学术会议

作者： ZHANG Li-hui~1,ZHAO Jian-bo~1,CHEN Wen-jian~1, YUAN Hui-ning~1,HU Quan~1,LIN Xiao-xia~1,FANG Zhi-ming~1,WEI Er-qing~2 (1.Department of Pharmacology,School of Basic Medicine,Hangzhou Normal University,Hangzhou 310036,China 2.Department of Pharmacology,School of Medicine,Zhejiang University,Hangzhou 310058,China)

pranlukast(ONO-1078) is a selective cysteinyl leukotriene receptor 1(CysLT1) ***, we have reported the protective efficacy of pranlukast on global cerebral ischemia in *** present study further evaluated dose-and time-dependent properties of pranlukast on delayed neuronal death of hippocampal CA1 neurons following transient global ischemia in rats and determined whether the effect of pranlukast is long *** ischemia was induced by an improved four-vessel occlusion(4-VO model) in ***(0.03,0.1 and 0.3 mg·kg) was injected intraperitoneally either as multiple doses or as a single dose,*** variables were monitored and neuron count was measured by computer-assisted *** transient global ischemia in rats causes selective and delayed neuronal death in the hippocampal CA1 *** were no significant differences in blood pressure,arterial blood pH,PO,PCO and blood glucose pre-ischemia and post-ischemia among the ***1 receptor antagonist pranlukast(0.1 and 0.3 mg·kg,30 min before ischemia and 1, 24,48 and 72 h after ischemia) markedly reduced hippocampal neuronal damage(Ppranlukast(0.1 mg·kg,30 min before ischemia) also resulted in a significant increase in the number of healthy CA1 neurons at 3 days after ischemia(Ppranlukast(0.1 mg·kg) rescued CA1 pyramidal neurons from ischemic death even when treatment was delayed until 30 min or 1 h after ischemia(Ppranlukast(0.1 mg·kg,7 consecutive days) is still evident 28 days after the ischemia episode,providing the experimental evident that CysLT1 receptor antagonists confer a long lasting *** present study confirms pranlukast has a dose-and time-dependent, and a long-lasting cerebroprotective effects on CA1 neuron loss following transient global ischemia in rats.

关键词： pranlukast cerebral ischemia delayed neuronal death hippocampal CA1 sector four-vessel occlusion neuroprotection

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沈阳药科大学学报 2008年第S1期25卷 55-55页

作者： ZHANG Li-hui1,ZHAO Jian-bo1,YUAN Hui-ning1,HU Quan1,WEI Er-qing2(1.Department of Pharmacology,Hangzhou Normal University,Hangzhou 310036,China 2.Department of Pharmacology,Zhejiang University,Hangzhou 310058,China)

Objective Our previous studies showed that the neuroprotective effect of pranlukast,a cysteinyl leukotriene receptor-1(CysLT1)antagonist,on global cerebral ischemia in *** study was performed to evaluate dose-and time-dependent properties of pranlukast on CA1 neuron loss following transient global ischemia in *** Brain injury was induced by an improved four-vessel occlusion(4-VO)in ***(0.03-0.30 mg·kg-1)was injected intraperitoneally either as multiple doses(before or after ischemia)or as a single dose(30 min before ischemia),*** variables were monitored and neuron count was measured by computer-assisted *** The 4-VO model produced continuing postischemic neuronal death in CA1 *** of pranlukast(0.1 and 0.3 mg·kg-1,30 min before ischemia and 1,24,48 and 72 h after ischemia)markedly reduced CA1 *** with a single dose of pranlukast(0.1 mg·kg-1,30 min before ischemia)also resulted in a significant increase in the number of healthy CA1 neurons at 3 *** interest is the finding that pranlukast(0.1 mg·kg-1)rescued CA1 neurons from ischemic death even when treatment was delayed until 30 min or 1 h after *** The present study confirms pranlukast has a dose-and time-dependent cerebroprotective effects on CA1 neuron loss following transient global ischemia in rats,with an effective dose range of 0.1-0.3 mg·kg-1 and a therapeutic window of 1 *** findings further support the therapeutic potential of CysLT1 receptor antagonists in the treatment of global cerebral ischemia.

关键词： pranlukast brain ischemia hippocampus neuroprotection

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pranlukast对脑损伤保护作用的研究进展

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浙江预防医学 2009年第1期21卷 65-66,68页

作者：张丽慧赵建波魏尔清杭州师范大学基础医学院浙江杭州310036 浙江大学医学院

pranlukast {SB 205312,pranlukast,4-氧-8-[对-(4-苯丁氧基)苯甲酰氨基]-2-(5-四氮基)-4H-1-苯并吡喃半水合物}是日本小野制药有限公司研制的半胱氨酰白三烯受体1(cysteinyl leukotriene receptor 1,CysLTRl)选择性拮抗剂,1995年3月获日本厚生省批准,同年6月在日本首次上市,1996年在欧洲和美国注册,已在临床用于治疗哮喘[1-2].近年来,越来越多的研究证明,pranlukast对多种脑损伤,如脑缺血、NMDA损伤及脑冷冻伤等有保护作用,提示具有治疗脑损伤潜在的应用价值.

关键词：脑损伤神经保护作用 pranlukast 神经元损伤脑缺血脑血管疾病海马脑片冷冻伤兴奋性氨基酸小鼠小家鼠局灶性剂量依赖性炎症介质化学介质大鼠原代神经元

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Cysteinyl leukotriene receptor 1 is involved in N-methyl-D-aspartate-mediated neuronal injury in mice

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Acta Pharmacologica Sinica 2006年第12期27卷 1526-1536页

作者： Qian DING Er-qing WEI~2 Yan-jun ZHANG Wei-ping ZHANG Zhong CHEN Department of Pharmacology,School of Medicine,Zhejiang University,Hangzhou 310058,China Department of Pharmacology School of Medicine Zhejiang University Hangzhou China

Aim:To determine whether cysteinyl leukotriene receptor 1(CysLT1receptor)isinvolved in N-methyl-D-aspartate(NMDA)-induced excitotoxic injury in the ***:Brain injury was induced by NMDA microinjection(50-150 nmolin 0.5 μL)into the cerebral *** changes in CysLT1receptor expression24 h after NMDA injection and the effects of a CysLT1receptor antagonist,pranlukast(0.01 and 0.1 mg/kg),an NMDA receptor antagonist,ketamine(30mg/kg),and an antioxidant,edaravone(9 mg/kg)were ***:In theNMDA-injured brain,the CysLT1receptor mRNA,and protein expression wereupregulated,and the receptor was mainly localized in the neurons and not in ***,ketamine and edaravone decreased NMDA-induced injury;pranlukast(0.1 mg/kg)and ketamine inhibited the upregulated expression of ***:CysLT1receptor expression in neurons isupregulated after NMDA injection,and NMDA-induced responses are inhibitedby CysLT1receptor antagonists,indicating that the increased CysLT1receptor isinvolved in NMDA excitotoxicity.

关键词： cysteinyl leukotriene receptor excitotoxicity N-methyl-D-aspartate leukotriene receptor antagonist pranlukast NMDA receptor antagonist ketamine

ONO-1078 reduces NMDA-induced brain injury and vascular cell adhesion molecule-1 expression in rats

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Acta Pharmacologica Sinica 2005年第4期26卷 435-440页

作者： Li-hui ZHANG~(2,3) Er-qing WEI~(2,4) 2 Department of Pharmacology,School of Medicine,Zhejiang University,Hangzhou 310031 3 Medical School,Hangzhou Normal University,Hangzhou 310018,China Department of Pharmacology School of Medicine Zhejiang University Hangzhou China Medical School Hangzhou Normal University Hangzhou China

Aim:To determine whether ONO-1078 （pranlukast）,a potent cysteinyl leukotrienereceptor 1 （CysLTI） antagonist,has an effect on N-methyl-D-aspartate （NMDA）-induced brain injury and vascular cell adhesion molecule-1 （VCAM-1） expres-sion in ***:Brain injury was induced by direct microinjection of NMDA（0.3 μmol in 1 μL of sterile 0.1 mol/L PBS,pH 7.4） into the cerebral *** volume （area）,brain edema and neuron density were assessed by an imageanalyzer and the expression of VCAM-1 in the cortex was detected by Westernblot 24 h after NMDA ***-1078 （0.03,0.1,or 0.3 mg/kg） andedaravone （MCI-186,10 mg/kg）,a neuroprotective agent,were ip injected 30rain before and after NMDA ***:NMDA microinjection producedwell-defined focal lesions （Figure 1） dose- and ***-1078（0.1,0.3 mg/kg） and edaravone （10 mg/kg） decreased the total lesion volume,lesion area and brain edema induced by ***,ONO-1078 （0.1,0.3mg/kg） significantly inhibited the enhanced expression of VCAM-1 in the injuredcortices,but edaravone did not have this ***:CysLT1receptorantagonist ONO-1078 at tenufftes NMDA-induced brain damage in rats,and thismight relate to the attenuation of NMDA receptor-dependent neurotoxicity andthe inhibition of the upregulation of VCAM-1 expression.

关键词： leukotriene antagonists pranlukast N-methylaspartate vascular cell adhesion molecule-1 neurotoxicity brain injuries