Rinsenoside Rg1 and its involvement in Hippo-YAP signaling pathway alleviating symptoms of depressive-like behavior

Area of Science:

• Neuroscience
• Pharmacology
• Cell Biology

Background:

• Chronic restraint stress (CRS) can induce anxiety and neuropathological changes.
• The antidepressant mechanisms of Ginsenoside Rg1 (G-Rg1) are not fully understood.
• The Hippo-YAP signaling pathway is implicated in stress-induced neuronal damage.

Purpose of the Study:

• To investigate the neuroprotective effects of G-Rg1 in a mouse model of CRS.
• To elucidate the role of the Hippo-YAP signaling pathway in G-Rg1's antidepressant action.
• To evaluate G-Rg1's impact on neuronal apoptosis and synaptic plasticity.

Main Methods:

• Sixty male C57BL/6 mice were allocated to control, CRS, and G-Rg1 treatment groups.
• PC12 cells were used to assess G-Rg1's effects on viability and apoptosis.
• Western blotting analyzed protein expression of the Hippo-YAP pathway components (p-YAP/YAP, p-MST1/MST1, p-LATS1/LATS1).

Main Results:

• G-Rg1 (5 and 10 mg/kg/day) alleviated behavioral and neuropathological changes in CRS mice.
• G-Rg1 treatment negatively correlated with activated Hippo-YAP pathway components in CRS mice.
• G-Rg1 inhibited corticosterone-induced apoptosis and Hippo-YAP pathway activation in PC12 cells.

Conclusions:

• Chronic G-Rg1 exhibits significant neuroprotective effects in both CRS mice and corticosterone-treated cells.
• Inhibition of the Hippo-YAP signaling pathway is a key mechanism for G-Rg1's neuroprotection.
• G-Rg1 reduces neuronal apoptosis and enhances synaptic plasticity, suggesting its potential as an antidepressant therapy.