Ginsenoside Rd reverses cognitive deficits by modulating BDNF-dependent CREB pathway in chronic restraint stress mice

Cognitive impairment has been widely recognized as a common symptom of chronic stress. Ginsenoside Rd (GRd), the major active compound in Panax ginseng, was previously reported in various neurological researches. However, little research is available regarding on the effect of GRd on cognitive impro...

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Bibliographic Details
Published in:Life sciences (1973) 2020-10, Vol.258, p.118107, Article 118107
Main Authors: Wang, Haixia, Jiang, Ning, Lv, Jingwei, Huang, Hong, Liu, Xinmin
Format: Article
Language:English
Subjects:
1-Phosphatidylinositol 3-kinase
Antioxidants
Brain-derived neurotrophic factor
Chronic restraint stress
Cognitive ability
Constraints
Cyclic AMP response element-binding protein
Ginseng
Ginsenoside Rd
Ginsenosides
Hippocampus
Impairment
Kinases
Learning and memory
Neuroprotection
Object recognition
Oral administration
Oxidative stress
Protein-tyrosine kinase
Signal transduction
Spontaneous alternation
TrkB receptors
Tyrosine
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Summary:Cognitive impairment has been widely recognized as a common symptom of chronic stress. Ginsenoside Rd (GRd), the major active compound in Panax ginseng, was previously reported in various neurological researches. However, little research is available regarding on the effect of GRd on cognitive improvement in mice subjected to chronic stress. In the present study, we investigated the neuroprotective effects of GRd in chronic restraint stress (CRS)-induced cognitive deficits and explored the potential mechanism in male C57BL/6J mice. Our results demonstrated that oral administration of GRd for 28 days markedly increased the spontaneous alternation in Y-maze and the relative discrimination index in novel object or location recognition tests following CRS. Additionally, GRd treatment considerably increased the antioxidant enzymes activities in the hippocampus. The expression levels of hippocampus and serum inflammation factors in the CRS groups were also counter-regulated by GRd treatment. Meanwhile, GRd treatment could reverse CRS-induced the decrease in phosphorylated phosphoinositide 3-kinase (PI3K), camp-reflecting element binding protein (CREB), brain-derived neurotrophic factor (BDNF) and tyrosine kinase B (TrkB) expression in the hippocampus. These findings provided evidences that GRd improves cognitive impairment in CRS mice by mitigating oxidative stress and inflammation, while upregulating the hippocampal BDNF-mediated CREB signaling pathway.
ISSN:0024-3205
1879-0631
DOI:10.1016/j.lfs.2020.118107