NDLI: Tripchlorolide Attenuates β-amyloid Generation via Suppressing PPARγ-Regulated BACE1 Activity in N2a/APP695 Cells

Content Provider	Springer Nature Link
Author	Lin, Nan Chen, Li min Pan, Xiao dong Zhu, Yuan gui Zhang, Jing Shi, Yan qing Chen, Xiao chun
Copyright Year	2015
Abstract	Due to its apparent rate-limiting function, BACE1 (β-secretase) appears to be a prime target for prevention of amyloid-β (Aβ) generation in brains with Alzheimer’s disease (AD). The activity of BACE1 is regulated by peroxisome proliferator-activated receptor-γ (PPARγ), a transcription factor binding site of the BACE1 promoter, indicating that PPARγ may be a potential target for AD treatment. Several studies have demonstrated that PPARγ activation is involved in the immunostimulation of amyloid-β precursor protein processing by nonsteroidal anti-inflammatory drugs (NSAIDs). The present study found that tripchlorolide (T$_{4}$), with a similar chemical structure to that of NSAIDs, decreased the levels of Aβ secreted in N2a-APP695 cells. T$_{4}$ treatment reduced the mRNA and protein levels of BACE1 and the protein level of sAPPβ, a cleaved N-terminal fragment of APP by BACE1. The treatment also translocated PPARγ from cytoplasm to nuclear. Intriguingly, T$_{4}$, like pioglitazone (a PPARγ agonist), suppressed the BACE1 activity in N2a-APP695 cells, which was attenuated by GW9662 (a PPARγ antagonist). These results indicate that T$_{4}$ may be a PPARγ agonist to enhance the binding of nuclear PPARγ to the BACE1 promoter, which may in turn inhibit the transcription and translation of BACE1, suppress the activity of BACE1, and ultimately attenuate the generation of Aβ. Due to its capability to alter Aβ generation and to protect central neural system against the neurotoxicity of Aβ, T$_{4}$ may serve as a promising agent in modulating Aβ-related pathology in Alzheimer’s disease.
Starting Page	6397
Ending Page	6406
Page Count	10
File Format	PDF
ISSN	08937648
Journal	Molecular Neurobiology
Volume Number	53
Issue Number	9
e-ISSN	15591182
Language	English
Publisher	Springer US
Publisher Date	2015-11-19
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Tripchlorolide Amyloid-β precursor protein Amyloidogenesis BACE1 PPARγ N2a cells Neurosciences Neurobiology Cell Biology Neurology
Content Type	Text
Resource Type	Article
Subject	Neurology Cellular and Molecular Neuroscience

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