Please use this identifier to cite or link to this item: https://ir.swu.ac.th/jspui/handle/123456789/12566
ชื่อเรื่อง: Bace1 inhibitor, neuroprotective, and neuritogenic activities of melatonin derivatives
ผู้แต่ง: Panyatip P.
Tadtong S.
Sousa E.
Puthongking P.
Keywords: acetylcholinesterase
amino acid
antifungal agent
antioxidant
beta secretase
beta secretase 1
glutathione peroxidase
glycine
melatonin derivative
neuroprotective agent
protein p19
quercetin
retinoic acid
tau protein
threonine
allosterism
Alzheimer disease
animal cell
Article
catalysis
cell viability
chemical structure
chloroplast
circular dichroism
controlled study
crystal structure
cytotoxicity
drug synthesis
Electrophorus electricus
enzyme activity
enzyme binding
fetal bovine serum
genetic algorithm
human
human cell
hydrogen bond
IC50
inflammation
molecular docking
molecular interaction
MTT assay
nerve cell
neurite outgrowth
neuroprotection
neurotoxicity
nonhuman
oxidative stress
quantitative structure activity relation
static electricity
วันที่เผยแพร่: 2020
บทคัดย่อ: Alzheimer’s disease (AD) is a common chronic neurodegenerative disorders. Melatonin (MLT) has been reported to be neuroprotective agent, and its modified structures exhibit potent antioxidant and anti-inflammation activities. Therefore, the activity of MLT and its derivatives against AD was investigated. Herein, the targeted enzymes, such as β-secretase (BACE1) and acetylcholinesterase (AChE), as well as the neuroprotective and neuritogenic effects on P19-derived neurons were evaluated. All the derivatives (1–5), including MLT, displayed potent inhibitory activity for BACE1, with inhibition values of more than 75% at 5 µM. A molecular docking study predicted that MLT, 5-MT, and 5 bound with BACE1 at catalytic amino acids Asp32 and the flap region, whereas 1–4 interacted with allosteric residue Thr232 and the flap region. The additional π-π interactions between 2, 3, and 5 with Tyr71 promoted ligand-enzyme binding. In addition, MLT, 1, 3, and 5 significantly protected neuron cells from oxidative stress by increasing the cell viability to 97.95, 74.29, 70.80, and 69.50% at 1 nM, respectively. Moreover, these derivatives significantly induced neurite outgrowth by increasing the neurite length and number. The derivatives 1, 3, and 5 should be thoroughly studied as potential AD treatment and neuroprotective agents. © 2020 by the authors. Licensee MDPI, Basel, Switzerland.
URI: https://ir.swu.ac.th/jspui/handle/123456789/12566
https://www.scopus.com/inward/record.uri?eid=2-s2.0-85098981013&doi=10.3390%2fscipharm88040058&partnerID=40&md5=044ee4dd1d631259cef60574c1facf99
ISSN: 368709
Appears in Collections:Scopus 1983-2021

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