Sodium Tanshinone IIA Sulfonate Improves Cognitive Impairment via Regulating Aβ Transportation in AD Transgenic Mouse Model

Alzheimer’s disease (AD) is a most common neurodegenerative disease. Sodium Tanshinone IIA Sulfonate (STS) has been reported to ameliorate AD pathology. However, the underlying mechanism is still unclear. In this study, APP/PS1 mouse model was used to explore the potential mechanism of STS against AD. Morris water maze and Y-maze tests showed that administration of STS (10 or 20 mg/kg/day) improved learning and memory abilities of APP/PS1 mice. STS reduced the levels of ROS and MDA, while improved the activity of SOD in both hippocampus and cortex in APP/PS1 mice. STS inhibited the activity of AChE, while improved the activity of ChAT in APP/PS1 mice. In addition, STS elevated the protein expressions of neurotrophic factors (BDNF and NGF) and synapse-related proteins (PSD93, PSD95 and SYP) in both the hippocampus and cortex in APP/PS1 mice. At last, STS improved the protein expressions of GLUT1 and LRP1. These results indicated that the potential mechanism of STS on AD might be related to Aβ transportation function via GLUT1/LRP1 pathway.