中国神经再生研究(英文版) ›› 2014, Vol. 9 ›› Issue (3): 252-259.doi: 10.4103/1673-5374.128217

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

减轻缺氧活化小胶质细胞介导神经元损伤的人参皂苷Rb1

  

  • 出版日期:2014-02-15 发布日期:2014-02-15
  • 基金资助:

    国家自然科学基金科学部主任基金资助项目(81041054);中国博士后科学基金面上资助项目(2013M542193)

Ginsenoside Rb1 attenuates activated microglia-induced neuronal damage

Lining Ke1, Wei Guo2, Jianwen Xu2, Guodong Zhang1, Wei Wang2, Wenhua Huang1   

  1. 1 Department of Human Anatomy, Histology and Embryology, Southern Medical University, Guangzhou, Guangdong Province, China
    2 Department of Human Anatomy, Histology and Embryology, Fujian Medical University, Fuzhou, Fujian Province, China
  • Online:2014-02-15 Published:2014-02-15
  • Contact: Wenhua Huang, M.D., Department of Human Anatomy, Histology and Embryology, Southern Medical University, Guangzhou 510515, Guangdong Province, China, huangwenhua2009@139.com. Wei Wang, M.D., Department of Human Anatomy, Histology and Embryology, Fujian Medical University, Fuzhou 350108, Fujian Province, China, wangwei0976@163.com.
  • Supported by:

    This study was supported by the National Natural Science Foundation of China, No. 81041054; China Postdoctoral Science Foundation funded project (General Program), No. 2013M542193.

摘要:

脑缺血缺氧时,活化态小胶质细胞介导的炎症反应促进了神经元损伤。以此推测,通过调控缺氧诱导的小胶质细胞的活化程度可能减轻神经元的损伤。为验证这个假说,实验以人参皂苷Rb1干预小胶质细胞与皮质神经元共培养体系,结果发现Rb1对神经元单独缺氧培养和与小胶质细胞共缺氧培养体系中的神经元形态结构的破坏有一定的保护作用,且能够在一定程度上减少单独缺氧培养和共缺氧培养体系中神经元的凋亡和Caspase-3的产量,其保护作用发挥在共培养之前;Rb1还可抑制含缺氧活化的小胶质细胞N9培养液的共培养体系中肿瘤坏死因子α的水平。无论是哪个细胞培养体系,Rb1均能够明显抑制缺氧诱导小胶质细胞N9产生的一氧化氮和O2-。提示人参皂苷Rb1可能通过下调缺氧活化的小胶质细胞中的一氧化氮、O2-、和肿瘤坏死因子α的表达,减轻大脑皮质神经元的损伤。

关键词: 神经再生, 中医药, 缺血缺氧, 小胶质细胞, 神经元, 细胞凋亡, 人参皂苷Rb1, 神经炎症因子, 基金资助文章

Abstract:

The microglia-mediated inflammatory reaction promotes neuronal damage under cerebral ischemia/hypoxia conditions. We therefore speculated that inhibition of hypoxia-induced microglial activation may alleviate neuronal damage. To test this hypothesis, we co-cultured ginsenoside Rb1, an active component of ginseng, and cortical neurons. Ginsenoside Rb1 protected neuronal morphology and structure in a single hypoxic culture system and in a hypoxic co-culture system with microglia, and reduced neuronal apoptosis and caspase-3 production. The protective effect was observable prior to placing in co-culture. Additionally, ginsenoside Rb1 inhibited levels of tumor necrosis factor-α in a co-culture system containing activated N9 microglial cells. Ginsenoside Rb1 also significantly decreased nitric oxide and superoxide production induced by N9 microglia. Our findings indicate that ginsenoside Rb1 attenuates damage to cerebral cortex neurons by downregulation of nitric oxide, superoxide, and tumor necrosis factor-α expression in hypoxia-activated microglia.

Key words: nerve regeneration, traditional Chinese medicine, ischemia/hypoxia, microglia, neurons, apoptosis, ginsenoside Rb1, nerve inflammation factor, NSFC grant, neural regeneration