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FA-97, a New Synthetic Caffeic Acid Phenethyl Ester Derivative, Protects against Oxidative Stress-Mediated Neuronal Cell Apoptosis and Scopolamine-Induced Cognitive Impairment by Activating Nrf2HO-1 Signaling
Joint Authors
Wang, Qi
Li, Wei-Rong
Mei, Yu
Wan, Ting
Wang, Zihao
Luo, Yi
Zhang, Yifan
He, Wei
Xue, Jincheng
Li, Min
Pan, Huafeng
Huang, Yujie
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2019, Issue 2019 (31 Dec. 2019), pp.1-21, 21 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2019-12-03
Country of Publication
Egypt
No. of Pages
21
Main Subjects
Abstract EN
Alzheimer’s disease (AD) is an age-related neurodegenerative disorder with cognitive deficits, which is becoming markedly more common in the world.
Currently, the exact cause of AD is still unclear, and no curative therapy is available for preventing or mitigating the disease progression.
Caffeic acid phenethyl ester (CAPE), a natural phenolic compound derived from honeybee hive propolis, has been reported as a potential therapeutic agent against AD, while its application is limited due to the low water solubility and poor bioavailability.
Here, caffeic acid phenethyl ester 4-O-glucoside (FA-97) is synthesized.
We validate that FA-97 attenuates H2O2-induced apoptosis in SH-SY5Y and PC12 cells and suppresses H2O2-induced oxidative stress by inhibiting the ROS level, malondialdehyde (MDA) level, and protein carbonylation level, as well as induces cellular glutathione (GSH) and superoxide dismutase (SOD).
Mechanistically, FA-97 promotes the nuclear translocation and transcriptional activity of Nrf2 associated with the upregulated expression of HO-1 and NQO-1.
The prime importance of Nrf2 activation in the neuroprotective and antioxidant effects of FA-97 is verified by Nrf2 siRNA transfection.
In addition, FA-97 prevents scopolamine- (SCOP-) induced learning and memory impairments in vivo via reducing neuronal apoptosis and protecting against cholinergic system dysfunction in the hippocampus and cortex.
Moreover, the increased MDA level and low total antioxidant capacity in SCOP-treated mouse brains are reversed by FA-97, with the increased expression of HO-1, NQO-1, and nuclear Nrf2.
In conclusion, FA-97 protects against oxidative stress-mediated neuronal cell apoptosis and SCOP-induced cognitive impairment by activating Nrf2/HO-1 signaling, which might be developed as a therapeutic drug for AD.
American Psychological Association (APA)
Wan, Ting& Wang, Zihao& Luo, Yi& Zhang, Yifan& He, Wei& Mei, Yu…[et al.]. 2019. FA-97, a New Synthetic Caffeic Acid Phenethyl Ester Derivative, Protects against Oxidative Stress-Mediated Neuronal Cell Apoptosis and Scopolamine-Induced Cognitive Impairment by Activating Nrf2HO-1 Signaling. Oxidative Medicine and Cellular Longevity،Vol. 2019, no. 2019, pp.1-21.
https://search.emarefa.net/detail/BIM-1205561
Modern Language Association (MLA)
Wan, Ting…[et al.]. FA-97, a New Synthetic Caffeic Acid Phenethyl Ester Derivative, Protects against Oxidative Stress-Mediated Neuronal Cell Apoptosis and Scopolamine-Induced Cognitive Impairment by Activating Nrf2HO-1 Signaling. Oxidative Medicine and Cellular Longevity No. 2019 (2019), pp.1-21.
https://search.emarefa.net/detail/BIM-1205561
American Medical Association (AMA)
Wan, Ting& Wang, Zihao& Luo, Yi& Zhang, Yifan& He, Wei& Mei, Yu…[et al.]. FA-97, a New Synthetic Caffeic Acid Phenethyl Ester Derivative, Protects against Oxidative Stress-Mediated Neuronal Cell Apoptosis and Scopolamine-Induced Cognitive Impairment by Activating Nrf2HO-1 Signaling. Oxidative Medicine and Cellular Longevity. 2019. Vol. 2019, no. 2019, pp.1-21.
https://search.emarefa.net/detail/BIM-1205561
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1205561