Neural Regeneration Research ›› 2014, Vol. 9 ›› Issue (3): 252-259.doi: 10.4103/1673-5374.128217

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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.

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