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Metformin restores the mitochondrial membrane potentials in association with a reduction in TIMM23 and NDUFS3 in MPP+-induced neurotoxicity in SH-SY5Y cells
SH-SY5Y cells exposed to 1-methyl-4-phenylpyridinium (MPP(+)) develop mitochondrial dysfunction and other cellular responses similar to those that occur in the dopaminergic neurons of patients with Parkinson's disease (PD). It has been shown in animal models of PD that neuronal death can be pre...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Leibniz Research Centre for Working Environment and Human Factors
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6806136/ https://www.ncbi.nlm.nih.gov/pubmed/31645842 http://dx.doi.org/10.17179/excli2019-1703 |
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author | Chanthammachat, Pitak Dharmasaroja, Permphan |
author_facet | Chanthammachat, Pitak Dharmasaroja, Permphan |
author_sort | Chanthammachat, Pitak |
collection | PubMed |
description | SH-SY5Y cells exposed to 1-methyl-4-phenylpyridinium (MPP(+)) develop mitochondrial dysfunction and other cellular responses similar to those that occur in the dopaminergic neurons of patients with Parkinson's disease (PD). It has been shown in animal models of PD that neuronal death can be prevented by metformin, an anti-diabetic drug. Both MPP(+) and metformin inhibit complex I of the mitochondrial respiratory chain. It has been reported that decreased levels of the mitochondrial inner membrane proteins TIMM23 and NDUFS3 are associated with the increased generation of reactive oxygen species and mitochondrial depolarization. In the present study, we investigated the effects of metformin on MPP(+)-induced neurotoxicity using differentiated human SH-SY5Y neuroblastoma cells. The results showed that pretreatment with metformin increased the viability of MPP(+)-treated SH-SY5Y cells. Pretreatment with metformin decreased the expression of TIMM23 and NDUFS3 in MPP(+)-treated SH-SY5Y cells. This was correlated with reduced mitochondrial fragmentation and an improvement in the mitochondrial membrane potential. These results suggest that metformin pretreatment protects against MPP(+)-induced neurotoxicity, and offer insights into the potential role of metformin in protecting against toxin-induced parkinsonism. |
format | Online Article Text |
id | pubmed-6806136 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Leibniz Research Centre for Working Environment and Human Factors |
record_format | MEDLINE/PubMed |
spelling | pubmed-68061362019-10-23 Metformin restores the mitochondrial membrane potentials in association with a reduction in TIMM23 and NDUFS3 in MPP+-induced neurotoxicity in SH-SY5Y cells Chanthammachat, Pitak Dharmasaroja, Permphan EXCLI J Original Article SH-SY5Y cells exposed to 1-methyl-4-phenylpyridinium (MPP(+)) develop mitochondrial dysfunction and other cellular responses similar to those that occur in the dopaminergic neurons of patients with Parkinson's disease (PD). It has been shown in animal models of PD that neuronal death can be prevented by metformin, an anti-diabetic drug. Both MPP(+) and metformin inhibit complex I of the mitochondrial respiratory chain. It has been reported that decreased levels of the mitochondrial inner membrane proteins TIMM23 and NDUFS3 are associated with the increased generation of reactive oxygen species and mitochondrial depolarization. In the present study, we investigated the effects of metformin on MPP(+)-induced neurotoxicity using differentiated human SH-SY5Y neuroblastoma cells. The results showed that pretreatment with metformin increased the viability of MPP(+)-treated SH-SY5Y cells. Pretreatment with metformin decreased the expression of TIMM23 and NDUFS3 in MPP(+)-treated SH-SY5Y cells. This was correlated with reduced mitochondrial fragmentation and an improvement in the mitochondrial membrane potential. These results suggest that metformin pretreatment protects against MPP(+)-induced neurotoxicity, and offer insights into the potential role of metformin in protecting against toxin-induced parkinsonism. Leibniz Research Centre for Working Environment and Human Factors 2019-09-10 /pmc/articles/PMC6806136/ /pubmed/31645842 http://dx.doi.org/10.17179/excli2019-1703 Text en Copyright © 2019 Chanthammachat et al. http://creativecommons.org/licenses/by/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Licence (http://creativecommons.org/licenses/by/4.0/) You are free to copy, distribute and transmit the work, provided the original author and source are credited. |
spellingShingle | Original Article Chanthammachat, Pitak Dharmasaroja, Permphan Metformin restores the mitochondrial membrane potentials in association with a reduction in TIMM23 and NDUFS3 in MPP+-induced neurotoxicity in SH-SY5Y cells |
title | Metformin restores the mitochondrial membrane potentials in association with a reduction in TIMM23 and NDUFS3 in MPP+-induced neurotoxicity in SH-SY5Y cells |
title_full | Metformin restores the mitochondrial membrane potentials in association with a reduction in TIMM23 and NDUFS3 in MPP+-induced neurotoxicity in SH-SY5Y cells |
title_fullStr | Metformin restores the mitochondrial membrane potentials in association with a reduction in TIMM23 and NDUFS3 in MPP+-induced neurotoxicity in SH-SY5Y cells |
title_full_unstemmed | Metformin restores the mitochondrial membrane potentials in association with a reduction in TIMM23 and NDUFS3 in MPP+-induced neurotoxicity in SH-SY5Y cells |
title_short | Metformin restores the mitochondrial membrane potentials in association with a reduction in TIMM23 and NDUFS3 in MPP+-induced neurotoxicity in SH-SY5Y cells |
title_sort | metformin restores the mitochondrial membrane potentials in association with a reduction in timm23 and ndufs3 in mpp+-induced neurotoxicity in sh-sy5y cells |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6806136/ https://www.ncbi.nlm.nih.gov/pubmed/31645842 http://dx.doi.org/10.17179/excli2019-1703 |
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