莫里斯水上航行任务
转基因小鼠
海马体
LRP1型
过剩1
氧化应激
突触可塑性
化学
药理学
转基因
神经科学
医学
内分泌学
生物化学
生物
葡萄糖转运蛋白
低密度脂蛋白受体
受体
脂蛋白
胆固醇
基因
胰岛素
作者
Huihan Ma,Can Wan,Ludi Zhang,Rongrong Zhang,Dong Peng,Lijun Qiao,Shijie Zhang,Yefeng Cai,Hongqiang Huang
标识
DOI:10.1007/s11011-022-00911-y
摘要
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 Aβ transportation function via GLUT1/LRP1 pathway. HIGHLIGHTS: STS improves cognitive impairment of APP/PS1 mice. STS ameliorates the oxidative stress damage and improves the cholinergic system. STS protects against neuronal dysfunction and enhances the synaptic plasticity. STS mediates the Aβ transportation of BMECs.
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