Please use this identifier to cite or link to this item: https://ir.swu.ac.th/jspui/handle/123456789/12719
ชื่อเรื่อง: Sesamin and sesamolin reduce amyloid-β toxicity in a transgenic Caenorhabditis elegans
ผู้แต่ง: Keowkase R.
Shoomarom N.
Bunargin W.
Sitthithaworn W.
Weerapreeyakul N.
Keywords: 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
วันที่เผยแพร่: 2018
บทคัดย่อ: 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
URI: https://ir.swu.ac.th/jspui/handle/123456789/12719
https://www.scopus.com/inward/record.uri?eid=2-s2.0-85051392264&doi=10.1016%2fj.biopha.2018.08.037&partnerID=40&md5=3233f9638d6d43da85f72b958f3a21f3
ISSN: 7533322
Appears in Collections:Scopus 1983-2021

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