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作 者:占成业[1] 熊杰[1] 周代星[1] 郑智[1] 邓普珍[1]
机构地区:[1]华中科技大学同济医学院附属同济医院急诊科,武汉430030
出 处:《临床急诊杂志》2004年第4期9-11,共3页Journal of Clinical Emergency
摘 要:目的:研究山莨菪对培养神经细胞谷氨酶兴奋毒性的作用。方法:体外培养新生SD大鼠皮层神经细胞,在谷氨酸处理神经细胞前后分别加入10^(-6)、10^(-4)mol/L的山莨若碱,观察山茛菪碱对谷氨酸所致神经细胞损伤的作用及对乳酸脱氢酶(LDH)、一氧化氮(NO)、丙二醛(MDA)和超氧化歧化酶(SOD)含量与活性的影响。结果:山莨菪碱能显著改善神经细胞受损的形态结构,减少细胞死亡数,降低LDH和NO含量,抑制MDA生成,提高SOD活性,且效应与药物浓度成正比。结论:山莨菪碱对体外培养神经细胞谷氨酸兴奋毒性具有明显的保护作用,其机制可能与抗脂质过氧化有关。Objeclive:To investigate the effects of anisodamine on glutamate excitotoxicity of neurons in vitro. Methods:The eorteal neu rons of new-born SD) rats were cultured and then treated with glutamate and anisodamine of 10^(-6) mol/Lor 10^(-4) mol/L. The effects of aniso damine on injury of neurons induced by glutamate and the contents of lactate dehydrogenase( LDH).nitric oxide(NO) and malondialdehyde (MDA) ,as well as the activities of superoxide dismutase(SOD) in cerebral cortical neuronal cuhures were observed.Results:Anisodamine relieved neurons injury, and reduced the number of cell death. Moreover, after treatment with anisodamine, the contents of LDH, NO and MDA dropped ,and the activities of SOD increased significantly. Conclusion:Anisodamine could protect cerebral cortical neurons from glutamate ex citotoxieity passibly by suppressing the generation of lipid peroxide.
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