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1- College of Public Health, Xinjiang Medical University, Urumqi, Xinjiang, China
Abstract:
Introduction: Alzheimer's Disease (AD) is a prevalent neurodegenerative disorder characterized by amyloid-beta (Aβ) accumulation, leading to inflammation, oxidative stress, and impaired synaptic function. This study explores the neuroprotective mechanisms of Vitis vinifera L. flavones (VTF) against Aβ-induced neurodegeneration and its potential as an AD therapeutic.
Methods: In an in vitro analysis, Aβ1-42 oligomers induced a mitophagy model in SH-SY5Y neuroblastoma cells. Cells were treated with VTF alone and in combination with chloroquine (CQ), a lysosome inhibitor, to assess Aβ1-42-induced mitophagy. Transmission electron microscopy (TEM) and Immunofluorescence (IFC) revealed Aβ1-42 effects on autophagosomes and deposition. Cellular protection against Aβ-induced damage was evaluated using the CCK-8 assay. Western blotting determined the expressions of autophagy–lysosomal pathway proteins (Beclin-1, Atg7, p62, and BACE1) and the LC3-II/LC3-I ratio as an autophagy marker.
Results: CQ and VTF demonstrated significant neuroprotection against Aβ1-42-induced neurodegeneration (P < 0.05). VTF, alone or with CQ, increased viable cell count (~1.2-fold; P < 0.05), indicating reparative capabilities. TEM and IFC showed robust protection by VTF and CQ against Aβ protein deposition and preservation of mitochondrial and autophagosomal structures. VTF and CQ treatments reduced Beclin-1, Atg7, and BACE1 levels, indicating modulation of Mitophagy and autophagy–lysosomal suppression. VTF+CQ maintained LC3-II/LC3-I balance, confirming VTF's role in preserving autophagy (P < 0.01).
Conclusions: This study unveils VTF's novel neuroprotective role, emphasizing its potential as an AD therapeutic. Future research should extend investigations to in vivo models and clinical settings, enhancing understanding of VTF's neuroprotective efficacy.
Methods: In an in vitro analysis, Aβ1-42 oligomers induced a mitophagy model in SH-SY5Y neuroblastoma cells. Cells were treated with VTF alone and in combination with chloroquine (CQ), a lysosome inhibitor, to assess Aβ1-42-induced mitophagy. Transmission electron microscopy (TEM) and Immunofluorescence (IFC) revealed Aβ1-42 effects on autophagosomes and deposition. Cellular protection against Aβ-induced damage was evaluated using the CCK-8 assay. Western blotting determined the expressions of autophagy–lysosomal pathway proteins (Beclin-1, Atg7, p62, and BACE1) and the LC3-II/LC3-I ratio as an autophagy marker.
Results: CQ and VTF demonstrated significant neuroprotection against Aβ1-42-induced neurodegeneration (P < 0.05). VTF, alone or with CQ, increased viable cell count (~1.2-fold; P < 0.05), indicating reparative capabilities. TEM and IFC showed robust protection by VTF and CQ against Aβ protein deposition and preservation of mitochondrial and autophagosomal structures. VTF and CQ treatments reduced Beclin-1, Atg7, and BACE1 levels, indicating modulation of Mitophagy and autophagy–lysosomal suppression. VTF+CQ maintained LC3-II/LC3-I balance, confirming VTF's role in preserving autophagy (P < 0.01).
Conclusions: This study unveils VTF's novel neuroprotective role, emphasizing its potential as an AD therapeutic. Future research should extend investigations to in vivo models and clinical settings, enhancing understanding of VTF's neuroprotective efficacy.
Keywords: Alzheimer's Disease, Vitis vinifera L. flavones, Chloroquine, Aβ1-42-induced neurodegeneration, Mitophagy, Neuroprotective efficacy
Type of Study: Original |
Subject:
Cellular and molecular Neuroscience
Received: 2024/05/19 | Accepted: 2024/12/4
Received: 2024/05/19 | Accepted: 2024/12/4
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