神经药理学报 ›› 2012, Vol. 2 ›› Issue (3): 7-14.

• 研究论文 • 上一篇    下一篇

蛇床子素对AD大鼠神经元凋亡及细胞周期的影响

董晓华1,孟宪勇2,张力1,杨建明1   

  1. 1. 河北北方学院药学系,张家口,075000,中国
    2. 河北北方学院附属第一医院,张家口,075000,中国
  • 出版日期:2012-06-26 发布日期:2013-12-25
  • 通讯作者: 张力,男,教授,硕士生导师;研究方向:神经药理学;Tel:+86-0313-4029188,E-mail:zmczl@hotmail.com
  • 作者简介:董晓华,女,副教授,博士;研究方向:神经药理学;Tel:+86-0313-4029305,E-mail:hbdxh76@163.com
  • 基金资助:

    河北省卫生厅资助项目(No.20090183),河北省科技厅资助项目(No.13272704D)

Effects of Osthole on Neuronal Apoptosis and Cell Cycle in AD Rats

DONG Xiao-hua1, MENG Xian-yong2, ZHANG Li1 , YANG Jian-ming1   

  1. 1. Department of Pharmacy, Hebei North University, Zhangjiakou, 075000, China 2. The First Attached Hospital, Hebei North University, Zhangjiakou, 075000, China
  • Online:2012-06-26 Published:2013-12-25
  • Contact: 张力,男,教授,硕士生导师;研究方向:神经药理学;Tel:+86-0313-4029188,E-mail:zmczl@hotmail.com
  • About author:董晓华,女,副教授,博士;研究方向:神经药理学;Tel:+86-0313-4029305,E-mail:hbdxh76@163.com
  • Supported by:

    河北省卫生厅资助项目(No.20090183),河北省科技厅资助项目(No.13272704D)

摘要: 目的:观察蛇床子素对阿尔茨海默病(Alzheimer's disease, AD)模型大鼠神经元凋亡及细胞周期的影响,探讨蛇床子素的神经保护作用及其作用机制。方法:采用一次性侧脑室注射聚集态β淀粉样肽(β-amyloid peptide,Aβ25-35)建立AD大鼠模型,腹腔注射12.5,25.0 mg·kg-1蛇床子素进行干预,观察大鼠认知功能、神经元凋亡及细胞周期变化。结果:蛇床子素能明显改善AD模型大鼠空间学习记忆能力,减少神经元凋亡,增加S期细胞百分率,促进G2/M期细胞进一步分裂,增强细胞增殖活性,调节细胞周期,有利于维持神经元正常的生理功能。结论:蛇床子素可通过减少神经元凋亡、调节细胞周期,具有神经保护作用,这可能是其改善AD大鼠学习记忆障碍的作用机制之一。

关键词: 蛇床子素, 阿尔茨海默病, 学习记忆, 神经元凋亡, 细胞周期

Abstract: Objective: To observe the influence of osthole on neuronal apoptosis and cell cycle in Alzheimer's disease (AD) rats and to study the neuroprotective effects and its mechanism. Methods: An intracerebroventricular (i.c.v.) injection of β-amyloid peptide (Aβ25-35) was administrated to establish AD rat model. Osthole(12.5,25.0 mg·kg-1) was injected intraperitoneally to rats and cognitive functions, neuronal apoptosis and cell cycle of AD rats were observed. Results: Osthole could improve spatial learning and memory abilities of AD rats, reduce neuronal apoptosis, increase the percentage of S phase cells, promote the G2/M phase cells to divide further, strengthen the cell proliferation activity, regulate cell cycle and benefit to the maintenance of normal physiological function of neurons. Conclusion: Osthole hasneuronal protection through reducing neuronal apoptosis and regulating cell cycle, which may be one of mechanism of improving learning and memory disorder in AD rats.

Key words: osthole, Alzheimer&, rsquo, s disease, learning and memory, neuronal apoptosis, cell cycle

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