Abstract: he aim of this study was to explore the effects of ginsenoside Rg1 on depression-like behaviors, hippocampal synaptic proteins and glial cell activation in stressed mice. Chronic unpredictable mild stress (CUMS) mice model was used to evaluate the effect of ginsenoside Rg1 ［10, 20, 40 mg/(kg·d), ip, 7 d］ on depression-like behaviors. The results showed that compared with control mice, sucrose preference index of CUMS mice decreased, immobility times was prolonged in the forced swimming and tail suspension experiments, which was prevented by Rg1 pretreatment. The expression of synaptic-related proteins PSD95 (postsynaptic density protein 95), Arc (activity-regulated cytoskeleton-associated protein) and BDNF (brain-derived neurotrophic factor) in the hippocampus of CUMS mice decreased, while the expression levels of astrocyte marker GFAP (glial fibrillary acidic protein), microglial marker Iba1 (ionized calcium binding adapter molecule 1) and inflammatory response factor NF-κB (nuclear factor kappa-B) increased. Administration of ginsenoside Rg1 ［20, 40 mg/(kg·d)］ increased the expression of hippocampal synaptic proteins, inhibited the activation of hippocampal astrocytes and microglia, and reduced the nuclear factor-κB (NF-κB) expression (vs CUMS， P<0.05). These data implicated that ginsenoside Rg1 prevents the depression-like behaviors likely through increasing the expression of hippocampal synaptic proteins and reducing activation of glial cells in CUMS mice.

Key words: depression, ginsenoside Rg1, synaptic plasticity, inflammation