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脱氢表雄酮对原代培养大鼠大脑皮质神经元谷氨酸释放的影响
引用本文:薛改,吴红海,侯艳宁. 脱氢表雄酮对原代培养大鼠大脑皮质神经元谷氨酸释放的影响[J]. 中国药学杂志, 2009, 44(4): 262-265
作者姓名:薛改  吴红海  侯艳宁
作者单位:1.中国人民解放军白求恩国际和平医院药学部 石家庄 050082;2.河北医科大学 石家庄 050017
基金项目:河北省自然科学基金资助项目(C2005000834)
摘    要: 目的观察脱氢表雄酮对大鼠大脑皮质神经元谷氨酸释放的影响。方法原代培养的SD大鼠大脑皮质神经元经不同浓度(1×10-7、1×10-6、1×10-5mol·L-1)和不同作用时间(0.5,1,1.5,2,5,24,36,48,72h)的脱氢表雄酮处理后,采用OPA-巯基乙醇柱前衍生,荧光检测-高效液相色谱法测定细胞培养液中谷氨酸的含量。结果与对照组相比,不同浓度的脱氢表雄酮处理后,细胞培养液中谷氨酸的水平均下降(P<0.05或P<0.01);与对照组相比,脱氢表雄酮处理组1,1.5,2,5,24,36,48,72h细胞培养液中谷氨酸的水平均下降(P<0.05或P<0.01)。结论脱氢表雄酮可抑制神经元谷氨酸的释放,这可能介导了其对抗谷氨酸兴奋性毒性的作用。

关 键 词:脱氢表雄酮  谷氨酸  大脑皮质
收稿时间:2008-02-03;

Effects of Dehydroepiandrosterone on Glutamate Released from Primary Cultured Rat Cerebral Cortical Neurons
XUE Gai,,WU Hong-hai,HOU Yan-ning. Effects of Dehydroepiandrosterone on Glutamate Released from Primary Cultured Rat Cerebral Cortical Neurons[J]. Chinese Pharmaceutical Journal, 2009, 44(4): 262-265
Authors:XUE Gai    WU Hong-hai  HOU Yan-ning
Affiliation:1. Deparment of Pharmacy,Bethune International Peace Hospital of PLA,Shijiazhuang 050082,China;2. Hebei Medical University,Shijiazhang 050017,China
Abstract:OBJECTIVE To investigate the effect of dehydroepiandrosterone on the levels of glutamate released from primary cultured rat cerebral cortical neurons. METHODS Primary cultured rat cerebral cortical neurons were treated with different concentrations(1×10-7,1×10-6,1×10-5mol·L-1) of dehydroepiandrosterone and the concentrations of glutamate in cell culture media at different times (0.5,1,1.5,2,5,24,36,48,72 h after treatment) were measured by OPA-mercaptoethanol precolumn derivatization technique and HPLC-FLD. RESULTS Compared with control group , different concentrations of dehydroepiandrosterone treatment significantly reduced the levels of glutamate(P<0.05 or P<0.01). Compared with control group,dehydroepiandrosterone treatment significantly reduced the levels of glutamate at 1,1.5,2,5,24,36,48,72 h(P<0.05 or P<0.01). CONCLUSION Dehydroepiandrosterone could inhibit the release of glutamate,which may mediate its role against excitotoxicity caused by glutamate.
Keywords:dehydroepiandrosterone  glutamate  cerebral cortex  neuron
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