| W-7对NMDA诱导的体外培养神经元凋亡的保护作用及机制 |
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| 引用本文： | 刘学文,胥向红,杨锐,贾玉洁. W-7对NMDA诱导的体外培养神经元凋亡的保护作用及机制[J]. 中国新药杂志, 2011, 0(14) |
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| 作者姓名： | 刘学文 胥向红 杨锐 贾玉洁 |
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| 作者单位： | 辽宁医学院附属第一医院神经内科;辽宁医学院; |
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| 基金项目： | 辽宁省科技厅博士启动基金(20091049) |
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| 摘 要： | 目的:观察钙调蛋白抑制剂N-(6-氨基己烷基)-5-氯-1萘-黄胺(W-7)对N-甲基-D-天冬氨酸(N-methyl-D-aspartic acid,NMDA)诱导的体外培养皮质神经元凋亡的影响,并探讨药物干预机制。方法:取原代培养7 d的大鼠皮质神经元随机分为5组:对照组,NMDA组,低(25μmo.lL-1)、中(50μmol.L-1)和高(100μmol.L-1)剂量W-7组。采用丫啶橙(acridine orange,AO)染色检测凋亡细胞数量;用免疫细胞化学染色法检测皮质神经元内p38丝裂原活化蛋白激酶(mitogen-activated protein kinase,MAPK)蛋白的表达。结果:与对照组比较,NMDA损伤组神经元凋亡明显增加(P<0.01);与NMDA组比较,W-7预处理组凋亡数量明显减少(P<0.05)。NMDA组p38MAPK蛋白表达显著增加(P<0.01),W-7干预组表达明显减少(P<0.05)。结论:W-7可减少NMDA诱导的神经元的凋亡,其作用机制可能是间接抑制p38MAPK的蛋白表达。
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| 关 键 词： | N-(6-氨基己烷基)-5-氯-1萘-黄胺(W-7) N-甲基-D-天冬氨酸 神经元凋亡 p38丝裂原活化蛋白激酶 |
Protective effect and mechanism of the calmodulin inhibitor W-7 on NMDA-induced apoptosis in cultured neurons |
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| LIU Xue-wen,XU Xiang-hong,YANG Rui,JIA Yu-jie. Protective effect and mechanism of the calmodulin inhibitor W-7 on NMDA-induced apoptosis in cultured neurons[J]. Chinese Journal of New Drugs, 2011, 0(14) |
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| Authors: | LIU Xue-wen XU Xiang-hong YANG Rui JIA Yu-jie |
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| Affiliation: | LIU Xue-wen1,XU Xiang-hong2,YANG Rui1,JIA Yu-jie1(1 Department of Neurology,the First Affiliated Hospital of Liaoning Medical College,Jinzhou 121001,China,2 Liaoning Medical College,China) |
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| Abstract: | Objective: To explore the protective effect of the calmodulin inhibitor W-7 on apoptosis indued by NMDA and the possible mechanisms in rat cortical neurons.Methods: Primary cortical neurons were cultured for 7 days before test.Apoptotic neurons were determined by acridine orange fluorescent staining.The expression of p38 MAPK protein was detected by immunocytochemistry.Results: Compared with control,the apoptotic neurons were significantly increased(P<0.01) after NMDA injury.Compared with NMDA alone,the num... |
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| Keywords: | W-7 NMDA neuron apoptosis p38 MAPK |
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