Publication:
Cratoxylum formosum Extract Protects against Amyloid-Beta Toxicity in a Caenorhabditis elegans Model of Alzheimer's Disease

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Issued Date

2016

Resource Type

Article

File Type

application/pdf

ISSN

320943

DOI

10.1055/s-0041-111621

Other identifier(s)

2-s2.0-84957705999

Rights Holder(s)

Scopus

Bibliographic Citation

Planta Medica. Vol 82, No.6 (2016), p.516-523

Suggested Citation

Keowkase R., Weerapreeyakul N. Cratoxylum formosum Extract Protects against Amyloid-Beta Toxicity in a Caenorhabditis elegans Model of Alzheimer's Disease. Planta Medica. Vol 82, No.6 (2016), p.516-523. doi:10.1055/s-0041-111621 Retrieved from: https://hdl.handle.net/20.500.14740/5486

Title

Cratoxylum formosum Extract Protects against Amyloid-Beta Toxicity in a Caenorhabditis elegans Model of Alzheimer's Disease

Author(s)

Keowkase R.
 Weerapreeyakul N.

Abstract

Amyloid-β, one of the hallmarks of Alzheimer's disease, is toxic to neurons and causes cell death in the brain. Oxidative stress is known to play an important role in Alzheimer's disease, and there is strong evidence linking oxidative stress to amyloid-β. The herbal plant Tiew kon (Cratoxylum formosum ssp. pruniflorum) is an indigenous vegetable that is grown in Southeast Asia. Many reports suggested that the twig extract from C. formosum possesses an antioxidant property. The purpose of this study was to investigate the protective effect of the twig extract from C. formosum against amyloid-β toxicity using the transgenic Caenorhabditis elegans model. This study demonstrated that the extract significantly delayed amyloid-β-induced paralysis in the C. elegans model of Alzheimer's disease. Using a genetic approach, we found that DAF-16/FOXO transcription factor, heat shock factor 1, and SKN-1 (Nrf2 in mammals) were required for the extract-mediated delayed paralysis. The extract ameliorated oxidative stress by reducing the level of H2O2, which appeared to account for the protective action of the extract. The extract possesses antioxidant activity against juglone-induced oxidative stress as it was shown to increase survival of the stressed worms. In addition, C. formosum decreased the expression of the heat shock protein-16.2 gene which was induced by thermal stress, indicating its ability to reduce cellular stress. The results from this study support the C. elegans model in the search for disease-modifying agents to treat Alzheimer's disease and indicate the potential of the extract from C. formosum ssp. pruniflorum as a source for the development of anti-Alzheimer's drugs. © Georg Thieme Verlag KG Stuttgart · New York.

Subject(s)

Amyloid beta protein
 Ascorbic acid
 Caffeic acid
 Chlorogenic acid
 Cratoxylum formosum extract
 Gallic acid
 Ginkgo biloba extract
 Heat shock transcription factor 1
 Hydrogen peroxide
 Juglone
 Neuroprotective agent
 Plant extract
 Transcription factor FOXO
 Transcription factor Nrf2
 Unclassified drug
 Amyloid beta protein
 Antioxidant
 Caenorhabditis elegans protein
 Daf-16 protein, C elegans
 DNA binding protein
 Forkhead transcription factor
 Heat shock factor-1, C elegans
 Naphthoquinone
 Plant extract
 Protective agent
 Skn-1 protein, C elegans
 Transcription factor
 Alzheimer disease
 Animal experiment
 Animal model
 Animal tissue
 Antioxidant activity
 Article
 Caenorhabditis elegans
 Cell stress
 Controlled study
 Cratoxylum formosum
 High performance liquid chromatography
 Neuroprotection
 Neurotoxicity
 Nonhuman
 Oxidative stress
 Paralysis
 Plant stem
 Plant twig
 Protein expression
 Quantitative analysis
 Survival
 Temperature stress
 Transgenic animal
 Alzheimer disease
 Animal
 Caenorhabditis elegans
 Chemistry
 Clusiaceae
 Disease model
 Drug effects
 Genetics
 Metabolism
 Paralysis
 Alzheimer Disease
 Amyloid beta-Peptides
 Animals
 Animals, Genetically Modified
 Antioxidants
 Caenorhabditis elegans
 Caenorhabditis elegans Proteins
 Clusiaceae
 Disease Models, Animal
 DNA-Binding Proteins
 Forkhead Transcription Factors
 Naphthoquinones
 Oxidative Stress
 Paralysis
 Plant Extracts
 Protective Agents
 Transcription Factors

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URI

https://hdl.handle.net/20.500.14740/5486

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Scopus: Year 1983-2021

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