Open AccessPassion fruit seed extract protects beta‐amyloid‐induced neuronal cell death in a differentiated human neuroblastoma SH‐SY5Y cell model
Author(s) -
Sato Akira,
Tagai Nozomi,
Ogino Yoko,
Uozumi Haruka,
Kawakami Shinpei,
Yamamoto Takayuki,
Tanuma Seiichi,
MarukiUchida Hiroko,
Mori Sadao,
Morita Minoru
Publication year - 2022
Publication title -
food science and nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.614
H-Index - 27
ISSN - 2048-7177
DOI - 10.1002/fsn3.2757
Subject(s) - piceatannol , neurite , neuroprotection , sh sy5y , programmed cell death , neurotrophic factors , neurotrophin , amyloid beta , microbiology and biotechnology , fragmentation (computing) , cell culture , cell , chemistry , neuroblastoma , biology , pharmacology , apoptosis , biochemistry , resveratrol , in vitro , receptor , peptide , genetics , ecology
Alzheimer's disease (AD) is a progressive neurodegenerative disease with accompanying perceptive disorder. We previously reported that decreasing levels of brain‐derived neurotrophic factor (BDNF) promoted beta‐amyloid (Aβ)‐induced neuronal cell death in neuron‐like differentiated SH‐SY5Y (ndSH‐SY5Y) human neuroblastoma cells in an AD mimic cell model. We investigated the neuroprotective effects of passion fruit seed extract (PFSE) and one of the main stilbene compounds, piceatannol, in an AD cell model using ndSH‐SY5Y cells. Both PFSE and piceatannol were found to protect Aβ‐induced neurite fragmentation in the cell model (protection efficacy; 34% in PFSE and 36% in piceatannol). In addition, both PFSE and piceatannol suppress Aβ‐induced neuronal cell death in the cell model (inhibitory effect; 27% in PFSE and 32% in piceatannol). Our study is the first to report that piceatannol‐rich PFSE can repress Aβ‐induced neuronal cell death by protecting against neurite fragmentation in the AD human cell model. These findings suggest that piceatannol‐rich PFSE can be considered a potentially neuroprotective functional food for both prevention and treatment of AD.