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

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

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 

作者机构:Department of Pharmacology School of Medicine Zhejiang University Hangzhou China Medical School Hangzhou Normal University Hangzhou China 

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

年 卷 期:2005年第26卷第4期

页      面:435-440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] 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(No 30271498) 

主  题:leukotriene antagonists pranlukast N-methylaspartate vascular cell adhesion molecule-1 neurotoxicity brain injuries 

摘      要: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.

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