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

2021 ◽  
Author(s):  
shijie zhang ◽  
Hui-Han Ma ◽  
Can Wan ◽  
Lu-Ding Zhang ◽  
Rong-Rong Zhang ◽  
...  
Keyword(s):  
Mouse Model ◽  
Underlying Mechanism ◽  
Transgenic Mouse Model ◽  
Tanshinone Iia ◽  
Potential Mechanism ◽  
Y Maze ◽  
Sodium Tanshinone Iia Sulfonate ◽  
Protein Expressions ◽  
Improved Learning ◽  
Related Proteins

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, 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.

scholarly journals Sodium tanshinone IIA sulfonate attenuates tumor oxidative stress and enhances apoptosis in an intermittent hypoxia mouse model

2019 ◽  
Author(s):  
Xiao-Bin Zhang ◽  
Xiao-Yang Chen ◽  
Xiao-Man Su ◽  
Hui-Qing Zeng ◽  
Yi-Ming Zeng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mouse Model ◽  
Western Blotting ◽  
Intermittent Hypoxia ◽  
Caspase 3 ◽  
Tanshinone Iia ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Related Factor ◽  
Obstructive Sleep ◽  
Sodium Tanshinone Iia Sulfonate

Abstract Objective The present study was designed to determine the effect of sodium tanshinone IIA sulfonate (TSA) on tumor oxidative stress and apoptosis in a mouse model of intermittent hypoxia (IH) which was considered a novel feature of obstructive sleep apnea. Materials and methods Mice were randomly assigned to control (normoxia) group (CTL), control plus TSA (CTL+TSA) group, IH group, and IH plus TSA (IH+TSA) group. The IH exposure lasted for 5 weeks. TSA was intraperitoneally injected in the CTL+TSA and IH+TSA group. Malondialdehyde (MDA) and superoxide dismutase (SOD) were detected for tumor oxidative stress levels. Terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay and western blotting of Bax, Cleaved Caspase-3 were conducted for evaluating tumor apoptotic levels. The expression levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and NF-κB were also evaluated by western blotting. Results Compared with the CTL group, mice exposed to the IH had higher MDA and lower SOD levels, and the TUNEL-positive cell rate, Bax and Cleaved Caspase-3 expressive levels were decreased in the IH group. The oxidative stress indexes were suppressed and the apoptotic levels were upregulated after treatment with TSA under the IH condition. The lower Nrf2 and higher NF-κB levels can be reversed by tretment with TSA under the IH condition. Conclusions The IH contributes to high oxidative stress and low apoptosis in tumor-bearing mice. TSA appears to improve IH-induced oxidative stress and apoptosis via Nrf2/NF-κB signaling pathway.

Rapamycin activates mitophagy and alleviates cognitive and synaptic plasticity deficits in a mouse model of Alzheimer’s disease

2021 ◽  
Author(s):  
Hui Wang ◽  
Jingxuan Fu ◽  
Xinxin Xu ◽  
Zhuo Yang ◽  
Tao Zhang
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Synaptic Plasticity ◽  
Mouse Model ◽  
Mitochondrial Function ◽  
Underlying Mechanism ◽  
Oxidative Status ◽  
Model Of Alzheimer’S Disease ◽  
Mouse Hippocampus ◽  
Related Proteins

Abstract Alzheimer’s disease (AD) is a chronic neurodegenerative disease, which is characterized by cognitive and synaptic plasticity damage. Rapamycin is an activator of autophagy/mitophagy, which plays an important role in identifying and degrading damaged mitochondria. The aim of this study was to investigate the effect of rapamycin on cognitive and synaptic plasticity defects induced by AD, and further explore if the underlying mechanism was associated with mitophagy. The results show that rapamycin increases parkin-mediated mitophagy and promotes fusion of mitophagosome and lysosome in the APP/PS1 mouse hippocampus. Rapamycin enhances learning and memory viability, synaptic plasticity and the expression of synapse related proteins, and impedes Cytochrome C-mediated apoptosis, decreases oxidative status and recovers mitochondrial function in APP/PS1 mice. The data suggest that rapamycin effectively alleviates AD-like behaviors and synaptic plasticity deficits in APP/PS1 mice, which is associated with enhanced mitophagy. Our findings possibly uncover an important function of mitophagy in eliminating damaged mitochondria to attenuate Alzheimer’s disease-associated pathology.

scholarly journals Sodium Tanshinone IIA Sulfonate Attenuates Scopolamine-Induced Cognitive Dysfunctions via Improving Cholinergic System

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Qing-Qing Xu ◽  
Yi-Jun Xu ◽  
Cong Yang ◽  
Ying Tang ◽  
Lin Li ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Escape Latency ◽  
Memory Deficit ◽  
Tanshinone Iia ◽  
Original Position ◽  
Oxygen Species ◽  
Neuroprotective Effects ◽  
Sodium Tanshinone Iia Sulfonate ◽  
Learning And Memory Deficit ◽  
Related Proteins

Sodium Tanshinone IIA sulfonate (STS) is a derivative of Tanshinone IIA (Tan IIA). Tan IIA has been reported to possess neuroprotective effects against Alzheimer’s disease (AD). However, whether STS possesses effect on AD remains unclear. This study aims to estimate whether STS could protect against scopolamine- (SCOP-) induced learning and memory deficit in Kunming mice. Morris water maze results showed that oral administration of STS (10 mg/kg and 20 mg/kg) and Donepezil shortened escape latency, increased crossing times of the original position of the platform, and increased the time spent in the target quadrant. STS decreased the activity of acetylcholinesterase (AChE) and increased the activity of choline acetyltransferase (ChAT) in the hippocampus and cortex of SCOP-treated mice. Oxidative stress results showed that STS increased the activity of superoxide dismutase (SOD) and decreased the levels of malondialdehyde (MDA) and reactive oxygen species (ROS) in hippocampus and cortex. In addition, western blot was carried out to detect the expression of apoptosis related proteins (Bcl-2, Bax, and Caspase-3). STS upregulated the protein expression of Bcl-2 and downregulated the proteins expression of Bax and Caspase-3. These results indicated that STS might become a promising therapeutic candidate for attenuating AD-like pathological dysfunction.

scholarly journals Therapeutic Effects of Human Amniotic Epithelial Stem Cells in a Transgenic Mouse Model of Alzheimer’s Disease

2020 ◽  
Vol 21 (7) ◽  
pp. 2658 ◽  
Author(s):  
Ka Kim ◽  
Yoo-Hun Suh ◽  
Keun-A Chang
Keyword(s):  
Stem Cells ◽  
Mouse Model ◽  
Transgenic Mouse ◽  
Water Maze ◽  
Amyloid Plaques ◽  
Transgenic Mouse Model ◽  
Therapeutic Effects ◽  
Epithelial Stem Cells ◽  
Maze Test ◽  
Y Maze

Alzheimer’s disease (AD), a progressive neurodegenerative disorder, is characterized clinically by cognitive decline and pathologically by the development of amyloid plaques. AD is the most common cause of dementia among older people. However, there is currently no cure for AD. In this study, we aimed to elucidate the therapeutic effects of human amniotic epithelial stem cells (hAESCs) in a transgenic mouse model of AD. Tg2576 transgenic (Tg) mice underwent behavioral tests, namely the Morris water maze and Y-maze tests, to assess their cognitive function. In the Morris water maze test, hAESC-treated Tg mice exhibited significantly shorter escape latencies than vehicle-treated Tg mice. In the Y-maze test, hAESC-treated Tg mice exhibited significantly higher rate of spontaneous alteration than vehicle-treated Tg mice, while the total number of arm entries did not differ between the groups. Furthermore, Congo red staining revealed that hAESCs injection reduced the number of amyloid plaques present in the brains of Tg mice. Finally, beta-secretase (BACE) activity was significantly decreased in Tg mice at 60 min after hAESCs injection. In this study, we found that intracerebral injection of hAESCs alleviated cognitive impairment in a Tg2576 mouse model of AD. Our results indicate that hAESCs injection reduced amyloid plaques caused by reduced BACE activity. These results indicate that hAESCs may be a useful therapeutic agent for the treatment of AD-related memory impairment.

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