Baicalin regulates depression behavior in mice exposed to chronic mild stress via the Rac/LIMK/cofilin pathway

Depression is a common disease that endangers people's physical and mental health. Traditional Chinese medicine has advantages in treating the emotional and cognitive symptoms of depressive disorders.

To study the effects of baicalin on the behavior and to clarify the underlying mechanism through evaluation of the Rac1-LIMK1-cofilin pathway.

A chronic mild stress (CMS) model of depression was used. Baicalin was administered to the mice for the intervention, and the positive control group was treated with fluoxetine. Behavioral tests were conducted to observe the degree of depressive disorders. Synaptophysin (SYP), postsynaptic density protein-95 (PSD95), brain-derived neurotrophic factor (BDNF), tyrosine kinase receptors (TrkB), Rac1 and cofilin expression was determined using Western blot analysis, and mRNA was quantified using real-time PCR.

Mice in the CMS group showed an increase in depression-like behavior (p <  0.01), while mice in the baicalin and fluoxetine groups showed a decrease in depression-like behavior (p <  0.01), compared with the control group. Electron microscopy showed ultrastructural changes in the hippocampal CA3 area of the CMS group, which were alleviated by baicalin treatment. SYP, PSD95, BDNF, TrkB, Rac1 and cofilin protein expression levels were decreased in the CMS group compared with the control group, while these levels were increased in the baicalin and fluoxetine groups (p <  0.01). There was no significant difference among the baicalin and fluoxetine groups (p >  0.05).

Baicalin markedly alleviated depression-like behavioral changes, exerted effects on SYP, PSD95, BDNF, and TrkB expression, activated the Rac1-cofilin pathway, and subsequently improve synaptic plasticity.