Effect of yuejuganmaidazaotang in hippocampus in postpartum depression model mice on AKT/mTOR signaling pathway

Aim: Using chronic pre-pregnancy stress to establish a postpartum depression animal model, given a single YG, and acute ketamine was served as control, to explore the pathology of PPD and the anti-depressive mechanism of the YG on the PPD model on AKT/ mTOR signaling pathway. Methods Thirty-two female Balb/c were randomly assigned to two groups, the control group (Control, Con) and the pre-pregnancy stressed group(Model,Mod) , which was subjected to 3 weeks chronic restraint stress. After the last stressor, the pre-pregnancy stressed group was housed with a male. After about 4 weeks later, the mice gave birth to pups. Then at 3 weeks postpartum, we tested the maternal tail suspension test (TST). Both YG and Ketamine was single administered 24 hours before behavior test, with single saline for control group and PPD model group. After TST, the mouse hippocampus were extracted to detect the expression of AKT and mTOR. Results: After 3 weeks postpartum, the model mice showed depression-like behaviors. Immobility in TST was significantly increased in vehicle groups (P < 0.01). Acute YG improved performance in the TST (P <0. 01) , which was similar to ketamine. And the PPD model mice group showed decreased phosphorylation of AKT and mTOR (P < 0. 01, P < 0. 01) , compared to control group. A single dose of YG or ketamine normalized AKT/mTOR signaling in the PPD model mice (P <0.0l,P <0.0l), (P <0.0l,P <0.0l). Conclusions: Chronic pre-pregnancy stress can induce dams into postpartum depression and its mechanism maybe associated with down-regulating AKT/mTOR signaling. Acute YG exerts fast antidepressant effect on this PPD model similar to ketamine, and its mechanism may be related to up-regulating AKT/mTOR signaling in the hippocampus.