Abstract:The effects of Jujuboside A (JuA) on the behavior and synaptic plasticity-related proteins in mouse models of depression were investigated. The depressive state of the mice was assessed through the tail suspension test (TST), forced swimming test (FST), open field test (OFT), and Morris water maze (MWM) test. Additionally, the expression levels of brain-derived neurotrophic factor (BDNF) in the hippocampus were determined using immunohistochemistry. Western blotting was then employed to assess the expression levels of tyrosine kinase receptor B (TrkB), cAMP responsive element binding (CREB), postsynaptic density protein 95 (PSD95), and autophagy effector protein Beclin1 (Beclin1). The results demonstrated that JuA significantly improved the depressive status in the mouse models. Furthermore, compared to the model group, the treatment group exhibited a substantial increase in the expression levels of BDNF (190.23%), TrkB (137.24%), CREB (76.29%), PSD95 (169.32%), and Beclin1 (82.53%) in the hippocampus post-JuA treatment. In summary, JuA exhibited substantial antidepressant effects on mice models of depression, significantly up-regulating the expression levels of hippocampal synaptic plasticity-related proteins, including BDNF, TrkB, CREB, PSD95, and Beclin1. This study establishes a theoretical foundation for the potential clinical application of JuA in treating depression. Additionally, it provides references for exploring therapeutic targets in pharmacy for depression.
