中国神经再生研究(英文版) ›› 2014, Vol. 9 ›› Issue (9): 943-950.doi: 10.4103/1673-5374.133137

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

人参皂苷Rb1干预对海马神经元损伤及突起生长的保护作用

  

  • 收稿日期:2014-04-03 出版日期:2014-05-20 发布日期:2014-05-20
  • 基金资助:

    国家自然科学基金(30971531, 81070987)

Neuroprotective effects of ginsenoside Rb1 on hippocampal neuronal injury and neurite outgrowth

Juan Liu, Jing He, Liang Huang, Ling Dou, Shuang Wu, Qionglan Yuan   

  1. Department of Anatomy and Neurobiology, Tongji University School of Medicine, Shanghai, China
  • Received:2014-04-03 Online:2014-05-20 Published:2014-05-20
  • Contact: Qionglan Yuan, Ph.D., Department of Anatomy and Neurobiology, Tongji University School of Medicine, Shanghai 200092, China, yqiongl@263.net.
  • Supported by:

    This work was supported by grants from the National Natural Science Foundation of China, No. 30971531, 81070987.

摘要:

人参皂苷Rb1具有抗老龄化和抗痴呆的神经保护作用,但对β-淀粉样蛋白所致的海马神经元损伤及神经突起生长受损可否能产生保护效应?实验以此为假设,旨在揭示是否参与神经突起生长和抵抗β淀粉样蛋白25-35所致海马神经元损伤的机制。结果显示,人参皂苷Rb1能促进培养的海马神经元突起生长,促进海马神经元p-Erk1/2和p-Akt蛋白表达,但分别加入Akt抑制剂API-2和MEK1/2抑制剂PD98059可抑制人参皂苷Rb1的上述作用。随后加入β淀粉样蛋白25-35处理30 min制备海马神经元损伤模型,发现Rb1显著逆转β淀粉样蛋白25-35所致海马神经元损伤后p-Akt和p-Erk1/2蛋白的下降,加入API-2可抑制人参皂苷Rb1的这一作用。说明人参皂苷Rb1促进海马神经元突起的生长,并抵抗β淀粉样蛋白25-35所致海马神经元损伤,其机制与Erk1/2和Akt信号通路有关。

关键词: 神经再生, 中医药, 人参皂苷Rb1, 海马神经元, 神经突起生长, 凋亡, 淀粉样β蛋白25-35, 生长相关蛋白-43, Hoechst33258染色, PD98059(MEK抑制剂), API-2(Akt 抑制剂), Erk1/2和Akt信号通路, 国家自然科学基金

Abstract:

Ginsenoside Rb1 has been reported to exert anti-aging and anti-neurodegenerative effects. In the present study, we investigate whether ginsenoside Rb1 is involved in neurite outgrowth and neuroprotection against damage induced by amyloid beta (25–35) in cultured hippocampal neurons, and explore the underlying mechanisms. Ginsenoside Rb1 significantly increased neurite outgrowth in hippocampal neurons, and increased the expression of phosphorylated-Akt and phosphorylated extracellular signal-regulated kinase 1/2. These effects were abrogated by API-2 and PD98059, inhibitors of the signaling proteins Akt and MEK. Additionally, cultured hippocampal neurons were exposed to amyloid beta (25–35) for 30 minutes; ginsenoside Rb1 prevented apoptosis induced by amyloid beta (25–35), and this effect was blocked by API-2 and PD98059. Furthermore, ginsenoside Rb1 significantly reversed the reduction in phosphorylated-Akt and phosphorylated extracellular signal-regulated kinase 1/2 levels induced by amyloid beta (25–35), and API-2 neutralized the effect of ginsenoside Rb1. The present results indicate that ginsenoside Rb1 enhances neurite outgrowth and protects against neurotoxicity induced by amyloid beta (25–35) via a mechanism involving Akt and extracellular signal-regulated kinase 1/2 signaling.

Key words: nerve regeneration, ginsenoside Rb1, hippocampal neurons, neurite outgrowth,  apoptosis, amyloid beta protein (25–35), growth-associated protein-43, Hoechst-33258 staining, PD98059, API-2, Akt and ERK1/2 signaling, NSFC grant, neural regeneration