Baicalin and ginsenoside Rb1 promote the proliferation and differentiation of neural stem cells in Alzheimer's disease model rats

Brain Res. 2018 Jan 1:1678:187-194. doi: 10.1016/j.brainres.2017.10.003. Epub 2017 Oct 14.

Abstract

Background: This study aimed to explore the effects of ginsenoside Rb1 and baicalin on the proliferation and differentiation of neural stem cells (NSC) in Alzheimer's disease model rats.

Method: The healthy Sprague Dawley male rats were randomly divided into 4 groups: control group, model group, ginsenoside Rb1 group and baicalin group. Besides, the animal model of dementia was induced by the injection of Aβ1-40. 2 weeks later, the rats in the baicalin and ginsenoside Rb1 groups were injected with baicalin and ginsenoside Rb1, respectively. The contents, expression sites of Nestin, GFAP and NSE and the percentage of viable cells were detected by immunohistochemistry. In addition, the expression levels of Nestin, GFAP and NSE in hippocampus of rats were detected by western-blot and metrology analysis was performed using quantity.

Results: Injection of Aβ1-40 significantly reduced the number of neuronal cells (p < .05). In addition, compared with the control group, the percentages of positive cells of NSCs, astrocytes and neuronal were increased. Besides, compared with the model group, the percentage of positive neural cells was improved by ginsenoside Rb1 (p < .05), and the percentages of astrocytes and neuronal were increased by ginsenoside Rb1 and baicalin (p < .05). Moreover, the expressions of Nestin and NSE were enhanced by ginsenoside Rb1 and baicalin (p < .05), while the GFAP level was only affected by ginsenoside Rb1 (p < .05) when compared with the model group.

Conclusion: Ginsenoside Rb1 and baicalin might promote the proliferation and differentiation of endogenous NSCs in AD rat model.

Keywords: Alzheimer’s disease; Baicalin; Ginsenoside Rb1; Neural stem cells.

MeSH terms

  • Alzheimer Disease / chemically induced
  • Alzheimer Disease / drug therapy
  • Amyloid beta-Peptides / toxicity
  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology*
  • Anti-Inflammatory Agents, Non-Steroidal / therapeutic use
  • Astrocytes / drug effects
  • Astrocytes / metabolism
  • Cell Differentiation / drug effects*
  • Cell Proliferation / drug effects*
  • Disease Models, Animal
  • Flavonoids / pharmacology*
  • Flavonoids / therapeutic use
  • Gene Expression Regulation / drug effects
  • Ginsenosides / pharmacology*
  • Ginsenosides / therapeutic use
  • Male
  • Nerve Tissue Proteins / metabolism
  • Neural Stem Cells / drug effects*
  • Neurons / drug effects
  • Neurons / metabolism
  • Peptide Fragments / toxicity
  • Rats
  • Rats, Sprague-Dawley

Substances

  • Amyloid beta-Peptides
  • Anti-Inflammatory Agents, Non-Steroidal
  • Flavonoids
  • Ginsenosides
  • Nerve Tissue Proteins
  • Peptide Fragments
  • amyloid beta-protein (1-40)
  • baicalin
  • ginsenoside Rb1