The calmodulin-dependent protein kinase II inhibitor KN-93 protects rat cerebral cortical neurons from N-methyl-D-aspartic acid-induced injury

查看全文 作　　者：Xuewen [1]Liu;Cui [2]Ma;Ruixian [1]Xing;Weiwei [3]Zhang;Buxian [1]Tian;Xidong [1]Li;Qiushi [1]Li;Yanhui [1]Zhang

机构地区：[1]Department of Neurology, First Affiliated Hospital of Liaoning Medical College;[2]Liaoning Medical College;[3]Jinzhou Kangning Hospital

出　　处：《Neural Regeneration Research》索引2013年第8卷第2期,共10页

基　　金：supported by Liaoning Social Development Key Projects of Scientific and Technological Department of Liaoning Province, No. 2012225019 摘　　要：In this study, primary cultured cerebral cortical neurons of Sprague-Dawley neonatal rats were treated with 0.25, 0.5, and 1.0 μM calmodulin-dependent protein kinase II inhibitor KN-93 after 50 μM N-methyl-D-aspartic acid-induced injury. Results showed that, compared with N-methyl-D-aspartic acid-induced injury neurons, the activity of cells markedly increased, apoptosis was significantly reduced, leakage of lactate dehydrogenase decreased, and intracellular Ca(2+) concentrations in neurons reduced after KN-93 treatment. The expression of caspase-3, phosphorylated calmodulin-dependent protein kinase II and total calmodulin-dependent protein kinase II protein decreased after KN-93 treatment. And the effect was apparent at a dose of 1.0 μM KN-93. Experimental findings suggest that KN-93 can induce a dose-dependent neuroprotective effect, and that the underlying mechanism may be related to the down-regulation of caspase-3 and calmodulin-dependent protein kinase II expression. 关键词：神经元损伤神经保护作用天门冬氨酸蛋白激酶钙调蛋白大脑皮质新生大鼠抑制剂

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The calmodulin-dependent protein kinase II inhibitor KN-93 protects rat cerebral cortical neurons from N-methyl-D-aspartic acid-induced injury

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