4.5 Article

Ginsenoside Rg3 exerts anti-depressive effect on an NMDA-treated cell model and a chronic mild stress animal model

Journal

JOURNAL OF PHARMACOLOGICAL SCIENCES
Volume 134, Issue 1, Pages 45-54

Publisher

JAPANESE PHARMACOLOGICAL SOC
DOI: 10.1016/j.jphs.2017.03.007

Keywords

Depression; Ginsenoside Rg3; HT22 cells; Chronic mild stress model

Funding

  1. National Natural Science Foundation of China [81202435]
  2. Guangdong Natural Science Foundation [2014A030307025]
  3. Special Fund for Public Welfare Research and Capacity Building in Guangdong Province [2016A020226021]
  4. High-Level Talent Project of Colleges and Universities In Guangdong Province [QBS201502]
  5. Sail Plan Foundation for High-Level Personnel Training Project of Guangdong
  6. Natural Science Foundation of Guangdong Province, China [2015A030313128]
  7. Key Science and Technology Project of Guangzhou Tianhe District, China [201404KW028]
  8. Science and Technology Project of Shenzhen City, China [JCYJ20150403151851068]

Ask authors/readers for more resources

Depression is a common mental disorder and a leading cause of disability. At its most severe, it can lead to suicide. Recently, there has been growing interest in the application of natural herbs for the prevention and treatment of depression. In this report, we found that the ginsenoside active component Rg3 has an apparent antidepressant effect. In N-methyl-D-aspartic acid (NMDA)-treated HT22 murine hippocampal neuronal cells, Rg3 recovered proliferation and inhibited apoptosis by altering the cell cycle. More interestingly, Rg3 led to apparent physiological behavior change in a chronic mild stress model as seen in forced swim, tail suspension, and sucrose preference tests. This effect was mediated by the phosphorylation of cAMP response element binding protein (CREB) and brain-derived neurotrophic factor (BDNF) signaling. This study provides direct evidence to support the antidepressant effects of ginsenoside Rg3, potentially indicating its application in the treatment of clinical depression. (C) 2017 The Authors. Production and hosting by Elsevier B.V. on behalf of Japanese Pharmacological Society.

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