文章摘要
张金波 宋汉君△ 刘爽 王淑秋 李鑫屹 吕冬霞 翟预珊.灵芝孢子粉对戊四氮活化海马神经细胞caspase-9 表达的研究[J].,2016,16(10):1850-1853
灵芝孢子粉对戊四氮活化海马神经细胞caspase-9 表达的研究
Study of Expression of Caspase-9 in Pentylenetetrazol Activation ofHippocampal Neurons by Ganoderma LucidumSpores
  
DOI:
中文关键词: 癫痫  细胞凋亡  神经元灵芝孢子粉
英文关键词: Epilepsy  Apoptosis  Neuron  Ganoderma lucidumspores
基金项目:佳木斯大学青年基金项目(Sq2012-38);佳木斯大学研究生科技创新项目(LZR2014_004)
作者单位
张金波 宋汉君△ 刘爽 王淑秋 李鑫屹 吕冬霞 翟预珊 佳木斯大学基础医学院 
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中文摘要:
      目的:本实验研究灵芝孢子粉对戊四氮活化大鼠海马神经细胞caspase-9表达变化的影响,进一步探索灵芝孢子粉对癫痫大 鼠脑保护的作用机制和癫痫与海马神经细胞凋亡调控基因之间的关系。方法:通过制备癫痫模型,RT-PCR 和Western blotting 检 测正常对照组、癫痫模型组和灵芝孢子粉用药组caspase-9 的表达。结果:癫痫模型组和灵芝孢子粉用药组caspase-9 的表达较正 常对照组均升高;其中癫痫模型组caspase-9 的表达水平与对照组比较明显升高,灵芝孢子粉用药组caspase-9 的表达水平与癫痫 模型组比较明显降低,差异有统计学意义。结论:本研究结果证实,Caspase-9介导了癫痫大鼠神经细胞凋亡机制,说明灵芝孢子 粉有效成份能充分作用于脑组织,可以调控caspase-9 的表达,发挥抗凋亡的神经保护作用。
英文摘要:
      Objective:This study is Ganoderma lucidum spores on pentylenetetrazol activation of caspase-9 expression change of rat hippocampal neurons to further explore the relationship between the action mechanismof the Ganoderma lucidumspores and epilepsy with apoptosis regulatory genes of hippocampal neural.Methods:Through the preparation of the epileptic model ,detection of caspase-9 expression by RT-PCR and Western blotting in the normal control group, epilepsy model group and Ganoderma spore powder medication group.Results:Caspase-9 expression in epilepsy model group and Ganoderma lucidum spores medication group were higher than in the normal control group; including caspase-9 expression level in epilepsy model group was significantly higher than in the control group, caspase-9 expression level in Ganoderma spore powder medication group were significantly lower than in epilepsy model group, the difference was statistically significant.Conclusion:This study of results confirmed that Caspase-9 mediates the mechanism of nerve cell apoptosis of epilepsy rats, it point active ingredients of Ganoderma spore powder can fully act on the brain tissue and regulate the expression of caspase-9 in order to play the role of anti-apoptotic neuroprotection.
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