Abstract
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.
Highlights
Alzheimer's disease (AD), a common neurodegenerative disorder, is characterized by progressive cognitive impairment and memory loss (Selkoe 2001)
Aβ plaques are considered as the main causes of AD, acting as a pathological trigger for a cascade such as oxidative stress, cholinergic system damage, synaptic dysfunction, and even neuronal damage loss
According to our previous study, in vivo we found that Sodium Tanshinone tanshinone IIA (IIA) Sulfonate (STS) can improve scopolamine-induced cognitive impairment and the damage of cholinergic system in mice (Xu Q.-Q. et al 2016), in vitro we found that STS could protect against Aβ - induced damage by modulating Aβ degradation and generation in SHSY5Y cell (Zhang et al 2020) and protect Aβ-induced injury by anti-apoptosis, anti-oxidative stress, relieving ER stress, and increasing the expression levels of IDE and NEP to clear Aβ in HT22 cell (Liu et al 2020)
Summary
Alzheimer's disease (AD), a common neurodegenerative disorder, is characterized by progressive cognitive impairment and memory loss (Selkoe 2001). As reported by Alzheimer’s Disease International, there was 50 million people suffered from AD in 2018. The number will reach to 15.2 billion in 2050. There is yet no suitable treatment for AD. Almost all phase III clinical trials targeting Aβ have failed (Kryscio et al 2017; Schott et al 2019; Sevigny et al 2016). It is urgent to find new drugs for AD treatment
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