Publication:
Sesamin and sesamolin reduce amyloid-β toxicity in a transgenic Caenorhabditis elegans

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Issued Date

2018

Resource Type

Article

File Type

application/pdf

ISSN

7533322

DOI

10.1016/j.biopha.2018.08.037

Other identifier(s)

2-s2.0-85051392264

Rights Holder(s)

มหาวิทยาลัยศรีนครินทรวิโรฒ

Bibliographic Citation

Biomedicine and Pharmacotherapy. Vol 107, (2018), p.656-664

Suggested Citation

Keowkase R., Shoomarom N., Bunargin W., Sitthithaworn W., Weerapreeyakul N. Sesamin and sesamolin reduce amyloid-β toxicity in a transgenic Caenorhabditis elegans. Biomedicine and Pharmacotherapy. Vol 107, (2018), p.656-664. doi:10.1016/j.biopha.2018.08.037 Retrieved from: https://hdl.handle.net/20.500.14740/5795

Title

Sesamin and sesamolin reduce amyloid-β toxicity in a transgenic Caenorhabditis elegans

Author(s)

Keowkase R.
 Shoomarom N.
 Bunargin W.
 Sitthithaworn W.
 Weerapreeyakul N.

Abstract

Alzheimer's disease (AD) is a devastating neurodegenerative disease characterized by β-amyloid (Aβ) plaques in the brain. At the present, there is no approved drug with a proven disease-modifying effect. Sesame seed (Sesame indicum) has long been known as a healthy food in Southeast Asian countries. Sesame lignans obtained from sesame seed possess antioxidant property that exhibit a variety of beneficial effects in various models. The objective of this study was to investigate the protective effects of sesame lignans including sesamin, sesamolin, and sesamol against Aβ toxicity in Caenorhabditis elegans (C. elegans) model of Aβ toxicity and to address whether these sesame lignans have a positive effect on lifespan extension. A transgenic C. elegans expressing human Aβ was used to investigate protective effects of sesame lignans against Aβ toxicity. Sesamin and sesamolin significantly alleviated Aβ-induced paralysis. The real-time PCR revealed that both sesamin and sesamolin did not affect the expression of Aβ transgene. However, we found that only sesamin inhibited Aβ oligomerization. These findings demonstrated that, among three sesame lignans tested, sesamin protected against Aβ toxicity by reducing toxic Aβ oligomers. Sesamin and sesamolin also significantly improved Aβ-induced defect in chemotaxis behavior and reversed the defect to normal. Moreover, sesamin prolonged median and mean lifespan of the wild type worm. On the other hand, sesamolin and sesamol failed to extend lifespan. These results offer valuable evidence for the future use of sesamin in the development of agents for the treatment of AD. It is also worth investigating the structure-activity relationship of lignan-related structures and their anti-Aβ toxicity activities in the future. © 2018 Elsevier Masson SAS

Subject(s)

Amyloid beta protein
 Dimethyl sulfoxide
 Ginkgo biloba extract
 Lignan derivative
 Oligomer
 Sesamin
 Sesamol
 Sesamolin
 Unclassified drug
 1,3 benzodioxole derivative
 1,3 dioxolane derivative
 Amyloid beta protein
 Lignan
 Phenol derivative
 Sesamin
 Sesamol
 Sesamolin
 Animal experiment
 Article
 Caenorhabditis elegans
 Chemotaxis
 Controlled study
 Drug effect
 Drug mechanism
 Gene expression
 Life extension
 Neuroprotection
 Neurotoxicity
 Nonhuman
 Oligomerization
 Priority journal
 Real time polymerase chain reaction
 Transgene
 Transgenic microorganism
 Wild type
 Animal
 Caenorhabditis elegans
 Chemistry
 Cytology
 Genetics
 Longevity
 Metabolism
 Nerve cell
 Paralysis
 Protein multimerization
 Transgenic animal
 Amyloid beta-Peptides
 Animals
 Animals, Genetically Modified
 Benzodioxoles
 Caenorhabditis elegans
 Chemotaxis
 Dioxoles
 Lignans
 Longevity
 Neurons
 Paralysis
 Phenols
 Protein Multimerization
 Transgenes

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URI

https://hdl.handle.net/20.500.14740/5795

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Scopus: Year 1983-2021

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