Sodium tanshinone IIA sulfonate improves cognitive impairment via regulating Aβ transportation in AD transgenic mouse model

Authors：Ma, Hui-Han; Wan, Can; Zhang, Lu-Di; Zhang, Rong-Rong; Peng, Dong; Qiao, Li-Jun; Zhang, Shi-Jie^*; Cai, Ye-Feng^*; Huang, Hong-Qiang^*

Source：Metabolic Brain Disease, 2022, 37(4): 989-1001.

DOI：10.1007/s11011-022-00911-y

• Alzheimer's disease
• Cognitive impairment
• Sodium Tanshinone IIA Sulfonate
• GLUT1
• LRP1

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, AD transgenic mouse model (APP/PS1) was used to explore the potential mechanism of STS against AD. Morris water maze and Y-maze tests showed that administration of STS improved learning and memory abilities of APP/PS1 mice. STS reduced the levels of reactive oxygen species and malondialdehyde, while improved the activity of superoxide dismutase in both hippocampus and cortex in APP/PS1 mice. STS inhibited the activity of acetylcholinesterase, while improved the activity of choline acetyltransferase in APP/PS1 mice. In addition, STS elevated the protein expressions of neurotrophic factors and synapse-related proteins in both the hippocampus and cortex in APP/PS1 mice. At last, STS improved the protein expressions of glucose transporter 1 (GLUT1) and low-density lipoprotein receptor-related protein 1 (LRP1). These results indicated that the potential mechanism of STS on AD might be related to A beta transportation function via GLUT1/LRP1 pathway.

• Institution
  广东省人民医院; 广州中医药大学