Effect of Plant Compound Curcumin on the Expression of SR-BI and ABCA1 in Hippocampal Neurons of APPswe/PS1dE9 Double Transgenic Mice

2013 ◽  
Vol 781-784 ◽  
pp. 1144-1147
Author(s):  
Jie Yun Sun ◽  
Zhi Peng Teng ◽  
Chen Wang ◽  
Ming Yuan Tian ◽  
Xiong Zhang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Hippocampal Neurons ◽  
Cholesterol Metabolism ◽  
Scavenger Receptor ◽  
Type I ◽  
Atp Binding Cassette Transporter ◽  
Class B ◽  
Double Transgenic Mice

Disorder of cholesterol metabolism plays important roles in pathogenesis of Alzheimer’s disease (AD). Plant compound curcumin has been reported to decrease Aβ deposition and cholesterol in serum, while the detailed mechanism is still unknown. To investigate the effect of curcumin on the cholesterol metabolism in Alzheimer’s disease, APPswe/PS1dE9 double transgenic mice were fed with 500ppm of curcumin every day for six months. Immunohistochemistryresults showed that the expression of ATP-binding cassette transporter A1 (ABCA1) in hippocampal neurons was increased significantly, whereas the expression of scavenger receptor class B type I (SR-BI) was not detected. These findings suggest that curcumin may promote cholesterol efflux via ABCA1 transmembrane-transport system rather than SR-BI in neurons of AD.

Effect of Plant Compound Curcumin on the Expression of a-Synuclein in Hippocampal Neurons of APPswe/PS1dE9 Double Transgenic Mice

2013 ◽  
Vol 781-784 ◽  
pp. 643-646
Author(s):  
Xiao Lin ◽  
Li Yu
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Hippocampal Neurons ◽  
Neuroprotective Effect ◽  
Disease Model ◽  
Dependent Manner ◽  
Double Transgenic Mice ◽  
Ad Alzheimer’S Disease ◽  
Dose Dependent

In this study, we aim to investigate the effect of curcumin on the expression of a-synuclein in the APPswe/PS1dE9 double transgenic mice. APPswe/PS1dE9 double transgenic mice were used as AD (Alzheimer's disease) model and fed with different concentrations of curcumin every day for 6 months, then immunohistochemistry method were used to detect the expression of a-synuclein in hippocampus of mice. The expression of a-syn in hippocampal neuron was decreased significantly after treated with 0.16g/kg to 1.0g/kg curcumin, the change was apparent in dose-dependent manner (P<0.05). a-synuclein pay an important role in the genesis and development of Alzheimer's disease and decreased level of a-synuclein might contribute to the neuroprotective effect of Curcumin, which may become a new target for the prevention and treatment of Alzheimer's disease.

Effects of Berberine on Expression of LOX-1 and SR-BI in Human Macrophage-Derived Foam Cells Induced by ox-LDL

2010 ◽  
Vol 38 (06) ◽  
pp. 1161-1169 ◽  
Author(s):  
Siming Guan ◽  
Bin Wang ◽  
Wei Li ◽  
Jinghuan Guan ◽  
Xin Fang
Keyword(s):  
Scavenger Receptor ◽  
Ldl Receptor ◽  
Foam Cells ◽  
Time Dependent ◽  
Human Macrophage ◽  
Type I ◽  
Dependent Manner ◽  
Atp Binding Cassette Transporter ◽  
Abca1 Expression ◽  
Class B

This study investigates the effects of beriberine on the expression of lectin-like ox-LDL receptor-1 (LOX-1), scavenger receptor A (SR-A), SR class B type I (SR-BI) and ATP-binding cassette transporter A1 (ABCA1) in human macrophage-derived foam cells induced by ox-LDL. Different concentrations of Berberine were co-cultured with THP-1 derived foam cells. The mRNA and protein expressions of LOX-1, SR-A, SR-BI and ABCA1 were determined by RT-PCR and Western blot analysis, respectively. Ox-LDL significantly increased the expression of LOX-1 and inhibited the expression of SR-BI in a dose- and time-dependent manner. Berberine significantly inhibited the effects of ox-LDL in a dose- and time-dependent manner. Moreover, ox-LDL significantly promoted ABCA1 expression. However, berberine had no effect on SR-A or ABCA1 expression. Berberine can inhibit the expression of LOX-1 and promote the expression of SR-BI in macrophage-derived foam cells. Therefore, berberine could be used to treat atherosclerotic diseases.

Increased ATP-Binding Cassette Transporter A1 Expression in Alzheimer's Disease Hippocampal Neurons

2010 ◽  
Vol 21 (1) ◽  
pp. 193-205 ◽  
Author(s):  
Woojin Scott Kim ◽  
Surabhi Bhatia ◽  
David A. Elliott ◽  
Lotta Agholme ◽  
Katarina Kågedal ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Hippocampal Neurons ◽  
Atp Binding ◽  
Atp Binding Cassette Transporter ◽  
Atp Binding Cassette

Cholesterol Metabolism—Impacts on SARS-CoV-2 Infection Prognosis, Entry, and Antiviral Therapies

2020 ◽  
Author(s):  
Congwen Wei ◽  
Luming Wan ◽  
Yanhong Zhang ◽  
Chen Fan ◽  
Qiulin Yan ◽  
...  
Keyword(s):  
Cholesterol Metabolism ◽  
Scavenger Receptor ◽  
Hdl Cholesterol ◽  
Lung Cells ◽  
Type I ◽  
Antiviral Therapies ◽  
Scavenger Receptor Class ◽  
Global Pandemic ◽  
Class B ◽  
Clinically Significant

AbstractThe recently emerged pathogenic SARS-coronavirus 2 (SARS-CoV-2) has spread rapidly, leading to a global pandemic. In this study, we show that SARS-CoV-2 infection was associated with clinically significant lower level of HDL cholesterol (HDL-C), which can be used as indicators of disease severity and poor prognosis. Importantly, we found the spike protein of SARS-CoV-2 (SARS-2-S) bound to HDL. Antagonists of HDL receptor-Scavenger receptor class B type I (SR-B1), strongly inhibited SARS-CoV-2 infection. Notably, the lipids transfer function of SR-B1 was indispensable for this inhibition, offering explanations for the reduced serum HDL level observed in COVID-19 patients. Basing on findings here, we speculate that SR-B1-mediated pulmonary HDL-vitamin E uptake could participate in mediating SARS-CoV-2 infection of lung cells, and the unique expression profile of SR-B1 may also affect SARS-CoV-2 cell and tissue tropism. These findings might help to provide further insights into viral transmission, pathological characteristics and reveal therapeutic targets.Graphical Abstract

scholarly journals Deposition of BACE-1 Protein in the Brains of APP/PS1 Double Transgenic Mice

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Gang Luo ◽  
Hongxia Xu ◽  
Yinuo Huang ◽  
Dapeng Mo ◽  
Ligang Song ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Protein Expression ◽  
Protein Accumulation ◽  
Significant Difference ◽  
Abnormal Accumulation ◽  
Double Transgenic Mice ◽  
Bace 1

The main causes of Alzheimer’s disease remain elusive. Previous data have implicated the BACE-1 protein as a central player in the pathogenesis of Alzheimer’s disease. However, many inhibitors of BACE-1 have failed during preclinical and clinical trials for AD treatment. Therefore, uncovering the exact role of BACE-1 in AD may have significant impact on the future development of therapeutic agents. Three- and six-month-old female APP/PS1 double transgenic mice were used to study abnormal accumulation of BACE-1 protein in brains of mice here. Immunofluorescence, immunohistochemistry, and western blot were performed to measure the distributing pattern and expression level of BACE-1. We found obvious BACE-1 protein accumulation in 3-month-old APP/PS1 mice, which had increased by the time of 6 months. Coimmunostaining results showed BACE-1 surrounded amyloid plaques in brain sections. The abnormal protein expression might not be attributable to the upregulation of BACE-1 protein, as no significant difference of protein expression was observed between wild-type and APP/PS1 mice. With antibodies against BACE-1 and CD31, we found a high immunoreactive density of BACE-1 protein on the outer layer of brain blood vessels. The aberrant distribution of BACE-1 in APP/PS1 mice suggests BACE-1 may be involved in the microvascular abnormality of AD.

scholarly journals Delta-secretase triggers Alzheimer’s disease pathologies in wild-type hAPP/hMAPT double transgenic mice

2020 ◽  
Vol 11 (12) ◽  
Author(s):  
Zhourui Wu ◽  
Xia Liu ◽  
Liming Cheng ◽  
Keqiang Ye
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Senile Plaques ◽  
Wild Type ◽  
Double Transgenic Mouse ◽  
Double Transgenic Mice ◽  
One Year ◽  
Aβ Production ◽  
Human Wild Type

AbstractAlzheimer’s disease (AD) is the most common neurodegenerative disease with multifactorial pathologies including Aβ containing senile plaques and neurofibrillary tangles (NFT) consisted of aggregated Tau. Most of the AD patients are sporadic and the familial mutation hereditary patients are composed only 1% of all cases. However, the current AD mouse models employ mutated APP, PS1, or even Tau mutant, in order to display a portion of AD pathologies. Delta-secretase (legumain, or asparaginyl endopeptidase, AEP) simultaneously cleaves both APP and Tau and augments Aβ production and Tau hyperphosphorylation and aggregation, contributing to AD pathogenesis. Here we show that δ-secretase is sufficient to promote prominent AD pathologies in wild-type hAPP/hMAPT double transgenic mice. We crossed hAPP l5 mice and hMAPT mice to generate double transgenic mouse model carrying both human wild-type APP and Tau. Compared to the single transgenic parents, these double transgenic mice demonstrated AD-related pathologies in one-year-old hAPP/hMAPT mice. Notably, overexpression of δ-secretase in hAPP/hMAPT double-transgenic mice evidently accelerated enormous senile plaques and NFT, associated with prominent synaptic defects and cognitive deficits. Hence, δ-secretase facilitates AD pathogenesis independent of any patient-derived mutation.

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