The antidepressant effects of Ginsenoside Rg1 and Rb1 are involved in regulating NMDAR1 phosphorylation via mTOR-Akt-NF-kappa B pathway in CUMS mouse model

[Speaker] Yan Liu:1,2
[Co-author] Yun-Long Zhang:1,2, Jun-Rong Zhu:1, Sui-Feng Liu:1,3, Lei Wen:1,2
1:Department of Traditional Chinese Medicine, Medical College, Xiamen University, China, 2:Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Medical College, Xiamen University, China, 3:Department of Cardiology, Zhongshan Hospital, Xiamen University, China

Depression is a common and serious mental illness which negatively affects people's feelings. Panax ginseng is widely used in treating the neurological disorders in the Far East, previously its active ingredients, including ginsenoside Rg1 and Rb1, have been demonstrated to ameliorate depression while the underlying mechanism is unclear. In the present study, we first explored the effects of ginsenoside Rg1 and Rb1 on chronic unpredictable mild stress (CUMS) induced depressive-like behaviors in mice, the results showed that ginsenoside Rg1 and Rb1 could reduce the immobility time in forced swimming and tail suspension tests. We further studied their effects on the glutamatergic synaptic transmission using molecular biological and electrophysiological approaches, the results demonstrated that both ginsenoside Rg1 and Rb1 could promote glutamate release in mouse prefrontal cortex and improve glutamatergic synaptic transmission by increasing the expression and function of glutamate receptors in the CUMS mouse model. The underlying mechanism is involved in ginsenoside Rg1 and Rb1 regulating the phosphorylation of NMDAR1 receptor via mTOR-Akt-NF-kappa B signaling pathway. These results indicate that ginsenoside Rg1 and Rb1 may serve as the potential agents against depression. Supported by the National Key Research and Development Program of China (No. 2016YFC1305903) and the grants from National Natural Science Foundation of China (No. 81373999 and No. 81774377).
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