PUBLICATION

The Neuroprotective Effects of Cyanidin Derivatives on AlCl3-Induced Zebrafish Model of Alzheimer's Disease

Authors
Wu, Y., Gao, Y., Tie, F., Wang, R., Hu, N., Dong, Q., Fu, C., Wang, H.
ID
ZDB-PUB-250927-26
Date
2025
Source
Molecules   30: (Journal)
Registered Authors
Keywords
Alzheimer’s disease, acetylcholinesterase, aluminum, cyanidin, molecular docking, zebrafish
MeSH Terms
  • Neuroprotective Agents*/chemistry
  • Neuroprotective Agents*/pharmacology
  • Humans
  • Alzheimer Disease*/chemically induced
  • Alzheimer Disease*/drug therapy
  • Alzheimer Disease*/metabolism
  • Alzheimer Disease*/pathology
  • Anthocyanins*/chemistry
  • Anthocyanins*/pharmacology
  • Animals
  • Aluminum Chloride/toxicity
  • Zebrafish
  • Molecular Dynamics Simulation
  • Molecular Docking Simulation
  • Oxidative Stress/drug effects
  • Brain/drug effects
  • Brain/metabolism
  • Brain/pathology
  • Acetylcholinesterase/chemistry
  • Acetylcholinesterase/metabolism
  • Disease Models, Animal
PubMed
41011582 Full text @ Molecules
Abstract
Alzheimer's disease (AD) is characterized by cholinergic deficits and neuronal damage, making acetylcholinesterase (AChE) a crucial therapeutic target. Cyanidin derivatives, sourced from the diet as anthocyanins, exhibit neuroprotective properties, yet comparative investigations are scarce. This research explored the neuroprotective impacts of five cyanidin derivatives, namely cyanidin-3-O-(trans-p-coumaroyl)-diglycoside (C3GG), cyanidin-3-O-rutinoside (C3R), cyanidin-3-O-arabinoside (C3A), cyanidin-3-O-sophoroside (C3S), and cyanidin-3-O-xyloside (C3X), utilizing an aluminum-chloride (AlCl3)-induced zebrafish model of AD. The administration of these compounds ameliorated zebrafish locomotor impairments, suppressed AChE activity, decreased brain oxidative stress levels, upregulated AD-related gene expression, and mitigated brain tissue pathological changes. Molecular docking and dynamics simulations indicated that cyanidin derivatives exhibit robust binding affinity and stable binding to AChE. Particularly, C3R demonstrated the most potent multi-faceted neuroprotective effects among the tested derivatives, suggesting its potential as a promising lead compound for AD therapy.
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