scholarly journals Ingredients in Zijuan Pu’er Tea Extract Alleviate β-Amyloid Peptide Toxicity in a Caenorhabditis elegans Model of Alzheimer’s Disease Likely through DAF-16

Molecules ◽  
2019 ◽  
Vol 24 (4) ◽  
pp. 729 ◽  
Author(s):  
Fangzhou Du ◽  
Lin Zhou ◽  
Yan Jiao ◽  
Shuju Bai ◽  
Lu Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Caenorhabditis Elegans ◽  
Protective Effect ◽  
Nuclear Translocation ◽  
Amyloid Β ◽  
Amyloid Peptide ◽  
C Elegans ◽  
Β Amyloid

Amyloid-β, one of the hallmarks of Alzheimer’s disease (AD), is toxic to neurons and can also cause brain cell death. Oxidative stress is known to play an important role in AD, and there is strong evidence that oxidative stress is associated with amyloid-β. In the present study we report the protective effect of Zijuan Pu’er tea water extract (ZTWE) and the mixture of main ingredients (+)-catechins, caffeine and procyanidin (MCCP) in ZTWE on β-amyloid-induced toxicity in transgenic Caenorhabditis elegans (C. elegans) CL4176 expressing the human Aβ1–42 gene. ZTWE, (+)-catechins, caffeine, procyanidin and MCCP delayed the β-amyloid-induced paralysis to different degrees. The MCCP treatment did not affect the transcript abundance of amyloid-β transgene (amy-1); however, Thioflavin T staining showed a significant decrease in Aβ accumulation compared to untreated worms. Further research using transgenic worms found that MCCP promoted the translocation of DAF-16 from cytoplasm to nucleus and increased the expression of superoxide dismutase 3 (SOD-3). In addition, MCCP decreased the reactive oxygen species (ROS) content and increased the SOD activity in CL4176 worms. In conclusion, the results suggested that MCCP had a significant protective effect on β-amyloid-induced toxicity in C. elegans by reducing β-amyloid aggregation and inducing DAF-16 nuclear translocation that could activate the downstream signal pathway and enhance resistance to oxidative stress.

scholarly journals AIP-1 ameliorates β-amyloid peptide toxicity in a Caenorhabditis elegans Alzheimer's disease model

2009 ◽  
Vol 18 (15) ◽  
pp. 2739-2747 ◽  
Author(s):  
Wail M. Hassan ◽  
David A. Merin ◽  
Virginia Fonte ◽  
Christopher D. Link
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Caenorhabditis Elegans ◽  
Disease Model ◽  
Amyloid Peptide ◽  
Β Amyloid ◽  
Β Amyloid Peptide

scholarly journals Fenton chemistry and oxidative stress mediate the toxicity of the β-amyloid peptide in aDrosophilamodel of Alzheimer’s disease

2009 ◽  
Vol 29 (7) ◽  
pp. 1335-1347 ◽  
Author(s):  
Thomas Rival ◽  
Richard M. Page ◽  
Dhianjali S. Chandraratna ◽  
Timothy J. Sendall ◽  
Edward Ryder ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Peptide ◽  
Fenton Chemistry ◽  
Β Amyloid ◽  
Β Amyloid Peptide ◽  
And Oxidative Stress

scholarly journals Effects of salvianolic acid A on β-amyloid mediated toxicity in Caenorhabditis elegans model of Alzheimer’s disease

2020 ◽  
Author(s):  
Chee Wah Yuen ◽  
Mardani Abdul Halim ◽  
Nazalan Najimudin ◽  
Ghows Azzam
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Caenorhabditis Elegans ◽  
Senile Plaques ◽  
Amyloid Peptide ◽  
Salvianolic Acid ◽  
Aggregation Effect ◽  
Salvianolic Acid A ◽  
Model Of Alzheimer’S Disease ◽  
Β Amyloid

AbstractAlzheimer’s disease (AD) is a brain disease attributed to the accumulation of extracellular senile plaques comprising β-amyloid peptide (Aβ). In this study, a transgenic Caenorhabditis elegans containing the human beta amyloid Aβ42 gene which exhibited paralysis when expressed, was used to study the anti-paralysis effect of salvianolic acid A. Various concentrations ranging from 1 μg/ml to 100 μg/ml of salvianolic acid A were tested and exhibited the highest effect on the worm at the concentration of 100 μg/ml. For anti-aggregation effect, 14 μg/ml salvianolic acid A (within 4 mg/ml of Danshen) showed a significant level of inhibition of the formation of Aβ fibrils. An amount of 100 μg/ml of salvianolic acid A had the potential in reducing the ROS but did not totally obliterate the ROS production in the worms. Salvianolic acid A was found to delay the paralysis of the transgenic C. elegans, decrease Aβ42 aggregation and decreased Aβ-induced oxidative stress.

scholarly journals Tocotrienol decreases β-amyloid mediated toxicity in Caenorhabditis elegans model of Alzheimer’s disease

2020 ◽  
Author(s):  
Chee Wah Yuen ◽  
Mardani Abdul Halim ◽  
Vikneswaran Murugaiyah ◽  
Nazalan Najimudin ◽  
Ghows Azzam
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Caenorhabditis Elegans ◽  
Senile Plaques ◽  
Amyloid Peptide ◽  
Model Of Alzheimer’S Disease ◽  
Aβ Aggregation ◽  
Anti Oxidant ◽  
Β Amyloid ◽  
Β Amyloid Peptide

AbstractAlzheimer’s disease (AD) is a neurological disease caused by the accumulation of extracellular senile plaques consisting of β-amyloid peptide (Aβ) in the brain. A transgenic Caenorhabditis elegans which demonstrated paralysis due to the expression of human beta amyloid Aβ42 gene was used to study the anti-paralysis effect of mixed tocotrienols. The content of the mixed tocotrienols were 12.1% α-, 2.7% β-, 18.6% γ-, and 8.1% δ-tocotrienols. Mixed tocotrienols significantly delayed the Aβ-induced paralysis in the transgenic nematode and exhibited anti-oxidant properties towards Aβ-generated oxidative stress. The mixture also presented potent inhibitory activities against Aβ aggregation with an IC50 value of 600 ng/ml. It is concluded that mixed tocotrienols could potentially serve as a new therapeutic candidate for AD.

Fucoidan inhibits amyloid-β-induced toxicity in transgenic Caenorhabditis elegans by reducing the accumulation of amyloid-β and decreasing the production of reactive oxygen species

2018 ◽  
Vol 9 (1) ◽  
pp. 552-560 ◽  
Author(s):  
Xuelian Wang ◽  
Kaixuan Yi ◽  
Yan Zhao
Keyword(s):  
Alzheimer’S Disease ◽  
Reactive Oxygen Species ◽  
Alzheimer's Disease ◽  
Caenorhabditis Elegans ◽  
Amyloid Β ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
C Elegans

Fucoidan treatment effectively alleviates the paralyzed phenotype induced by the accumulation of Abeta in a transgenic Caenorhabditis elegans (C. elegans) Alzheimer's disease (AD) model.

scholarly journals Sideritis scardica extracts inhibit aggregation and toxicity of amyloid-β in Caenorhabditis elegans used as a model for Alzheimer's disease

2017 ◽  
Author(s):  
Felix Heiner ◽  
Björn Feistel ◽  
Michael Wink
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Caenorhabditis Elegans ◽  
Pharmacological Activity ◽  
Model Organism ◽  
Amyloid Β ◽  
Ethanolic Extract ◽  
Active Principle ◽  
Head Region ◽  
C Elegans

Background. Beyond its traditional uses in the Balkan area, Sideritis scardica (known as Greek mountain tea, Lamiaceae) is currently extensively investigated for its pharmacological activity in the central nervous system. Antidepressant, psychostimulating, cognition-enhancing and neuroprotective properties have been described. In this study, we tested hydroalcoholic extracts of S. scardica for their potential to counteract amyloid-β toxicity and aggregation, which plays a crucial role in the pathogenesis of Alzheimer's disease. Methods. For this purpose, we have chosen the nematode Caenorhabditis elegans, which is used as a model organism for neurodegenerative diseases. The concentration of different polyphenols in extracts prepared from water, 20, 40, 50, and 70 % ethanol was analysed by HPLC. Additionally, polar and unpolar fractions were prepared from the 40 % ethanolic extract and phytochemically analysed. Results. Essentially, the contents of all measured constituents increased with the lipophilicity of the extraction solvents. Treatment of transgenic C. elegans strains expressing amyloid-β with the extracts resulted in a reduced number of peptide aggregates in the head region of the worms and alleviated toxicity of amyloid-β, observable through the degree of paralysed animals. The mid-polar extracts (40 and 50 % ethanol) turned out be the most active, decreasing the plaque number by 21 % and delaying the amyloid-β-induced paralysis by up to 3.5 h. The more lipophilic extract fractions exhibited higher activity than the hydrophilic ones. Discussion. Sideritis scardica extracts demonstrated pharmacological activity against characteristics of Alzheimer's disease also in C. elegans, supporting current efforts to assess its potential for the treatment of cognitive decline. The active principle as well as the mode of action needs to be investigated in more detail.

scholarly journals Sideritis scardica extracts inhibit aggregation and toxicity of amyloid-β in Caenorhabditis elegans used as a model for Alzheimer's disease

2017 ◽  
Author(s):  
Felix Heiner ◽  
Björn Feistel ◽  
Michael Wink
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Caenorhabditis Elegans ◽  
Pharmacological Activity ◽  
Model Organism ◽  
Amyloid Β ◽  
Ethanolic Extract ◽  
Active Principle ◽  
Head Region ◽  
C Elegans

Background. Beyond its traditional uses in the Balkan area, Sideritis scardica (known as Greek mountain tea, Lamiaceae) is currently extensively investigated for its pharmacological activity in the central nervous system. Antidepressant, psychostimulating, cognition-enhancing and neuroprotective properties have been described. In this study, we tested hydroalcoholic extracts of S. scardica for their potential to counteract amyloid-β toxicity and aggregation, which plays a crucial role in the pathogenesis of Alzheimer's disease. Methods. For this purpose, we have chosen the nematode Caenorhabditis elegans, which is used as a model organism for neurodegenerative diseases. The concentration of different polyphenols in extracts prepared from water, 20, 40, 50, and 70 % ethanol was analysed by HPLC. Additionally, polar and unpolar fractions were prepared from the 40 % ethanolic extract and phytochemically analysed. Results. Essentially, the contents of all measured constituents increased with the lipophilicity of the extraction solvents. Treatment of transgenic C. elegans strains expressing amyloid-β with the extracts resulted in a reduced number of peptide aggregates in the head region of the worms and alleviated toxicity of amyloid-β, observable through the degree of paralysed animals. The mid-polar extracts (40 and 50 % ethanol) turned out be the most active, decreasing the plaque number by 21 % and delaying the amyloid-β-induced paralysis by up to 3.5 h. The more lipophilic extract fractions exhibited higher activity than the hydrophilic ones. Discussion. Sideritis scardica extracts demonstrated pharmacological activity against characteristics of Alzheimer's disease also in C. elegans, supporting current efforts to assess its potential for the treatment of cognitive decline. The active principle as well as the mode of action needs to be investigated in more detail.

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