机构：[1]School of Basic Medical Sciences, Kunming Medical University, Kunming 650500, P. R. China,[2]Library, Yunnan Minzu University, Kunming 650500, P. R. China,[3]School of Pharmaceutical Sciences, Department of Zoology & Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming Medical University, Kunming 650500, P. R. China,[4]First affiliated hospital of Kunming medical university, Kunming 650000, P. R. China昆明医科大学附属第一医院[5]Institute of Molecular Clinical Medicine, Kunming Medical University, Kunming 650000, P. R. China[6]Yunnan University of Traditional Chinese Medicine, Kunming, Yunnan 650500, P. R. China
Depression-like behaviors caused by chronic stress are related to inflammation and microglia
activation. Antidepressant therapy may contribute to inhibiting inflammation responses and
microglia activation. Ginsenoside Rb1 (GRb1) is known to display antidepressant-like effect on
chronic unpredictable mild stress-induced depressive rats. However, the antidepressant-like
effects of GRb1 on chronic restraint stress (CRS) mice and the potential anti-inflammatory
mechanisms are unclear. Here, we focused on the molecular mechanisms related to inhibition
of inflammation response and the protection on microglia. Our results showed that GRb1 had
an antidepressant effects via relieving the depression-like behaviors in CRS model. Furthermore,
GRb1 increased the protein expressions of brain-derived neurotrophic factor and phosphoprotein kinase B/ protein kinase B (p-AKT/AKT), and decreased the protein expressions of
interleukin-1β (IL-1β), tumor necrosis factor α (TNF-α) and ionized calcium binding adapter
molecule 1 in hippocampus, reduced the levels IL-1β and TNF-α in serum. Finally, GRb1
lowered the protein expressions of IL-1β and TNF-α in BV-2 microglia induced by
lipopolysaccharides. Taken together, the results indicate that GRb1 prevents CRS-induced
depression-like behaviors in mice, which may be related to anti-inflammatory effects in
hippocampus, serum and microglia and activation of AKT pathway.
基金：
This work was supported by “Yun Ling Scholars”, Applied Basic Research Key Project
of Yunnan (Grant Agreement No. 2019FA033, 2019FA031), Applied Basic Research
Project of Yunnan (Grant Agreement No.202001AT070137), Toxic Medicinal Plants
Research Innovation Team of Yunnan Province (Grant Agreement No. 2020HC008), and National Natural Science Foundation of China (Grant Agreement No. 82060650,31900290).
