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中国临床药理学与治疗学 ›› 2003, Vol. 8 ›› Issue (3): 273-277.

• 研究原著 • 上一篇    下一篇

人参皂苷Rg1 可能通过抗氧化作用来保护帕金森病鼠黑质神经元1

周宜灿, 陈晓春, 朱元贵, 陈丽敏, 方芳   

  1. 福建医科大学附属协和医院, 福建省老年医学研究所, 福州 350001, 福建
  • 收稿日期:2002-12-24 修回日期:2003-01-08 出版日期:2003-06-26 发布日期:2020-11-25
  • 通讯作者: 陈晓春, 男, 教授, 博士生导师, 研究方向:神经系统变性疾病的发病机理。Tel:0591-3377664 E-mail:xc-chen329@sohu.com
  • 作者简介:周宜灿, 男, 医学硕士。
  • 基金资助:
    1 福建省科技厅和教育厅科学研究项目基金资助课题(№;2001Z037,JA02219)

Down-regulation of oxidative stress is the possible mechanism of ginsenoside Rg1 protecting the substantia nigra neurons in PD mice1

ZHOU Yi-Can, CHEN Xiao-Chun, ZHU Yuan-Gui, FANG Fang, CHEN Li-Min   

  1. Fujian Institute of Geriatrics, Union Hospital, Fujian Medical University, Fuzhou 350001, Fujian
  • Received:2002-12-24 Revised:2003-01-08 Online:2003-06-26 Published:2020-11-25

摘要: 目的: 研究人参皂苷Rg1 对1-甲基-4-苯基-1, 2, 3, 6-四氢吡啶(1-methyl-4-phenyl-1, 2, 3, 6- tetrahydropyridine, MPTP)诱导的小鼠黑质神经元凋亡的抗氧化保护作用。方法: 采用MPTP 制备帕金森病(PD)小鼠模型, 经人参皂苷Rg1 预处理后, 用尼氏(Nissl)染色和TH 组化染色观察黑质神经元的存活情况, 通过活化型Caspase 3 的免疫组化染色和TUNEL 染色了解黑质神经元的凋亡情况, 并用生化技术对黑质区域谷胱甘肽(GSH)浓度及超氧化物歧化酶(SOD)活力进行检测。结果: 人参皂苷Rg1 预处理能提高黑质区域GSH 的浓度及降低SOD 活力,相应地减少PD 鼠黑质致密带Nissl 阳性神经元和TH 阳性神经元的脱失现象, 使活化型Caspase 3 表达阳性细胞减少, 降低黑质神经元TUNEL 染色的阳性率。结论: 人参皂苷Rg1 可能对MPTP 诱导的小鼠黑质神经元凋亡有抗氧化保护作用。

关键词: 药效学, 人参皂苷Rg1, 凋亡, 黑质神经元, 氧化应激

Abstract: AIM: To explore the role of ginsenoside Rg1 as an antioxidant in preventing against 1-methyl-4- phenyl-1, 2, 3, 6- tetrahydropyridine (MPTP)-induced apoptosis of substantia nigra neurons in Parkinson' s disease (PD)mice models. METHODS: C57BL mice were administrated (sc)withMPTP to produce PD mice models.Different doses (5.0, 10.0, and 20.0 mg·kg -1)of Rg1 were given (ip)MPTP prior 3 days in the pretreatment groups.Nissl staining, tyrosinehydroxythase (TH) immunostaining, cleaved caspase 3 immunostaining, and TUNEL staining were used to observe the changes of nigra neurons.Meanwhile, biochemical technique was used to detect the concentration of GSH and the vitality of SOD in substantia nigra. RESULTS: Pretreatment with Rg1 could increase the concentration of GSH and descent the vitality of SOD in substantia nigra, prevent the loss of Nissl staining neurons and TH-positive neurons, and decrease the percent of cleaved caspase 3 and TUNEL-positive cells. CONCLUSION: Down-regulation of oxidative stress is the possible mechanism of ginsenoside Rg1 protecting the substantia nigra neurons in PD mice.

Key words: pharmacodynamics, ginsenoside Rg1, apoptosis, substantia nigra neuron, oxidative stress

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