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Quercetin alleviates high glucose-induced Schwann cell damage by autophagy

Quercetin can reverse high glucose-induced inhibition of neural cell proliferation, and therefore may have a neuroprotective effect in diabetic peripheral neuropathy. It is difficult to obtain primary Schwann cells and RSC96 cells could replace primary Schwann cells in studies of the role of autopha...

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Detalles Bibliográficos
Autores principales: Qu, Ling, Liang, Xiaochun, Gu, Bei, Liu, Wei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medknow Publications & Media Pvt Ltd 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4146282/
https://www.ncbi.nlm.nih.gov/pubmed/25206782
http://dx.doi.org/10.4103/1673-5374.135328
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author Qu, Ling
Liang, Xiaochun
Gu, Bei
Liu, Wei
author_facet Qu, Ling
Liang, Xiaochun
Gu, Bei
Liu, Wei
author_sort Qu, Ling
collection PubMed
description Quercetin can reverse high glucose-induced inhibition of neural cell proliferation, and therefore may have a neuroprotective effect in diabetic peripheral neuropathy. It is difficult to obtain primary Schwann cells and RSC96 cells could replace primary Schwann cells in studies of the role of autophagy in the mechanism underlying diabetic peripheral neuropathy. Here, we show that under high glucose conditions, there are fewer autophagosomes in immortalized rat RSC96 cells and primary rat Schwann cells than under control conditions, the proliferative activity of both cell types is significantly impaired, and the expression of Beclin-1 and LC3, the molecular markers for autophagy, is significantly lower. After intervention with quercetin, the autophagic and proliferative activity of both cell types is rescued. These results suggest that quercetin can alleviate high glucose-induced damage to Schwann cells by autophagy.
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spelling pubmed-41462822014-09-09 Quercetin alleviates high glucose-induced Schwann cell damage by autophagy Qu, Ling Liang, Xiaochun Gu, Bei Liu, Wei Neural Regen Res Research and Report Quercetin can reverse high glucose-induced inhibition of neural cell proliferation, and therefore may have a neuroprotective effect in diabetic peripheral neuropathy. It is difficult to obtain primary Schwann cells and RSC96 cells could replace primary Schwann cells in studies of the role of autophagy in the mechanism underlying diabetic peripheral neuropathy. Here, we show that under high glucose conditions, there are fewer autophagosomes in immortalized rat RSC96 cells and primary rat Schwann cells than under control conditions, the proliferative activity of both cell types is significantly impaired, and the expression of Beclin-1 and LC3, the molecular markers for autophagy, is significantly lower. After intervention with quercetin, the autophagic and proliferative activity of both cell types is rescued. These results suggest that quercetin can alleviate high glucose-induced damage to Schwann cells by autophagy. Medknow Publications & Media Pvt Ltd 2014-06-15 /pmc/articles/PMC4146282/ /pubmed/25206782 http://dx.doi.org/10.4103/1673-5374.135328 Text en Copyright: © Neural Regeneration Research http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research and Report
Qu, Ling
Liang, Xiaochun
Gu, Bei
Liu, Wei
Quercetin alleviates high glucose-induced Schwann cell damage by autophagy
title Quercetin alleviates high glucose-induced Schwann cell damage by autophagy
title_full Quercetin alleviates high glucose-induced Schwann cell damage by autophagy
title_fullStr Quercetin alleviates high glucose-induced Schwann cell damage by autophagy
title_full_unstemmed Quercetin alleviates high glucose-induced Schwann cell damage by autophagy
title_short Quercetin alleviates high glucose-induced Schwann cell damage by autophagy
title_sort quercetin alleviates high glucose-induced schwann cell damage by autophagy
topic Research and Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4146282/
https://www.ncbi.nlm.nih.gov/pubmed/25206782
http://dx.doi.org/10.4103/1673-5374.135328
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