Troxerutin flavonoid has neuroprotective properties and increases neurite outgrowth and migration of neural stem cells from the subventricular zone.
Amyloid beta-Protein Precursor
/ pharmacology
Animals
Astrocytes
/ metabolism
Cell Differentiation
/ drug effects
Cell Movement
/ drug effects
Cell Proliferation
/ drug effects
Cells, Cultured
Flavonoids
/ pharmacology
Hydroxyethylrutoside
/ analogs & derivatives
Lateral Ventricles
/ drug effects
Male
Mice
Mice, Inbred BALB C
Neural Stem Cells
/ drug effects
Neurites
/ drug effects
Neurogenesis
Neuronal Outgrowth
/ physiology
Neurons
/ metabolism
Neuroprotection
Neuroprotective Agents
/ metabolism
Journal
PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081
Informations de publication
Date de publication:
2020
2020
Historique:
received:
18
03
2020
accepted:
17
07
2020
entrez:
16
8
2020
pubmed:
17
8
2020
medline:
27
10
2020
Statut:
epublish
Résumé
Troxerutin (TRX) is a water-soluble flavonoid which occurs commonly in the edible plants. Recent studies state that TRX improves the functionality of the nervous system and neutralizes Amyloid-ß induced neuronal toxicity. In this study, an in vitro assay based upon Neural stem cell (NSCs) isolated from the subventricular zone of the postnatal balb/c mice was established to explore the impact of TRX on individual neurogenesis processes in general and neuroprotective effect against ß-amyloid 1-42 (Aß42) induced inhibition in differentiation in particular. NSCs were identified exploiting immunostaining of the NSCs markers. Neurosphere clonogenic assay and BrdU/Ki67 immunostaining were employed to unravel the impact of TRX on proliferation. Differentiation experiments were carried out for a time span lasting from 48 h to 7 days utilizing ß-tubulin III and GFAP as neuronal and astrocyte marker respectively. Protective effects of TRX on Aß42 induced depression of NSCs differentiation were determined after 48 h of application. A neurosphere migration assay was carried out for 24 h in the presence and absence of TRX. Interestingly, TRX enhanced neuronal differentiation of NSCs in a dose-dependent manner after 48 h and 7 days of incubation and significantly enhanced neurite growth. A higher concentration of TRX also neutralized the inhibitory effects of Aß42 on neurite outgrowth and length after 48 h of incubation. TRX significantly stimulated cell migration. Overall, TRX not only promoted NSCs differentiation and migration but also neutralized the inhibitory effects of Aß42 on NSCs. TRX, therefore, offers an interesting lead structure from the perspective of drug design especially to promote neurogenesis in neurological disorders i.e. Alzheimer's disease.
Identifiants
pubmed: 32797057
doi: 10.1371/journal.pone.0237025
pii: PONE-D-20-07816
pmc: PMC7428079
doi:
Substances chimiques
Amyloid beta-Protein Precursor
0
Flavonoids
0
Hydroxyethylrutoside
0
Neuroprotective Agents
0
troxerutin
7Y4N11PXO8
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e0237025Déclaration de conflit d'intérêts
The authors have read the journal’s policy and have the following potential competing interests: PM is a paid employee of Ursapharm Arzneimittel GmbH. This does not alter our adherence to PLOS ONE policies on sharing data and materials. There are no patents, products in development or marketed products associated with this research to declare.
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