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Pioglitazone protects PC12 cells against oxidative stress injury: An in vitro study of its antiapoptotic effects via the PPARγ pathway

To the best of our knowledge, the role of peroxisome proliferator-activated receptor γ (PPARγ) in oxidative stress-induced PC12 cell damage is unknown. Using a PC12 cell model with H(2)O(2) treatment, the present study investigated the expression levels of apoptosis-related genes and neuronal apopto...

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Autores principales: Li, Yali, Long, Jun, Li, Libo, Yu, Ziyao, Liang, Yanjing, Hou, Bin, Xiang, Li, Niu, Xiaolin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10580242/
https://www.ncbi.nlm.nih.gov/pubmed/37854503
http://dx.doi.org/10.3892/etm.2023.12221
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author Li, Yali
Long, Jun
Li, Libo
Yu, Ziyao
Liang, Yanjing
Hou, Bin
Xiang, Li
Niu, Xiaolin
author_facet Li, Yali
Long, Jun
Li, Libo
Yu, Ziyao
Liang, Yanjing
Hou, Bin
Xiang, Li
Niu, Xiaolin
author_sort Li, Yali
collection PubMed
description To the best of our knowledge, the role of peroxisome proliferator-activated receptor γ (PPARγ) in oxidative stress-induced PC12 cell damage is unknown. Using a PC12 cell model with H(2)O(2) treatment, the present study investigated the expression levels of apoptosis-related genes and neuronal apoptosis after oxidative stress injury. The present study further investigated the protective effect and mechanism of pioglitazone, a PPARγ agonist. PC12 cells treated with H(2)O(2) were used as a model of oxidative stress injury. An MTT assay and flow cytometry were used to detect the effect of H(2)O(2) on PC12 cell viability and the protective effect of pioglitazone. A TUNEL assay was used to detect neuronal apoptosis. The expression levels of PPARγ, Bax, Bcl-2 and caspase-3 were examined by reverse transcription-quantitative PCR and western blotting. H(2)O(2) reduced PC12 cell viability in a dose- and time-dependent manner. H(2)O(2) significantly upregulated the protein expression levels of Bax and the cleaved caspase-3/caspase-3 ratio (P<0.01), decreased the protein expression levels of Bcl-2 (P<0.01), and increased the apoptosis rate of PC12 cells. Pioglitazone significantly reduced the protein expression levels of Bax and the cleaved caspase-3/caspase-3 ratio (P<0.01), increased the expression levels of Bcl-2 (P<0.01), decreased the Bax/Bcl-2 expression ratio (P<0.01) and increased the viability of H(2)O(2)-damaged PC12 cells in a dose-dependent manner. Treatment with the PPARγ antagonist GW9662 or PPARγ small interfering RNA counteracted the protective effect of pioglitazone on PC12 cells to different extents (P<0.01). Therefore, the present study reported the role of PPARγ in protecting PC12 cells against oxidative stress injury, which may lead to novel therapeutic approaches for neurodegenerative diseases.
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spelling pubmed-105802422023-10-18 Pioglitazone protects PC12 cells against oxidative stress injury: An in vitro study of its antiapoptotic effects via the PPARγ pathway Li, Yali Long, Jun Li, Libo Yu, Ziyao Liang, Yanjing Hou, Bin Xiang, Li Niu, Xiaolin Exp Ther Med Articles To the best of our knowledge, the role of peroxisome proliferator-activated receptor γ (PPARγ) in oxidative stress-induced PC12 cell damage is unknown. Using a PC12 cell model with H(2)O(2) treatment, the present study investigated the expression levels of apoptosis-related genes and neuronal apoptosis after oxidative stress injury. The present study further investigated the protective effect and mechanism of pioglitazone, a PPARγ agonist. PC12 cells treated with H(2)O(2) were used as a model of oxidative stress injury. An MTT assay and flow cytometry were used to detect the effect of H(2)O(2) on PC12 cell viability and the protective effect of pioglitazone. A TUNEL assay was used to detect neuronal apoptosis. The expression levels of PPARγ, Bax, Bcl-2 and caspase-3 were examined by reverse transcription-quantitative PCR and western blotting. H(2)O(2) reduced PC12 cell viability in a dose- and time-dependent manner. H(2)O(2) significantly upregulated the protein expression levels of Bax and the cleaved caspase-3/caspase-3 ratio (P<0.01), decreased the protein expression levels of Bcl-2 (P<0.01), and increased the apoptosis rate of PC12 cells. Pioglitazone significantly reduced the protein expression levels of Bax and the cleaved caspase-3/caspase-3 ratio (P<0.01), increased the expression levels of Bcl-2 (P<0.01), decreased the Bax/Bcl-2 expression ratio (P<0.01) and increased the viability of H(2)O(2)-damaged PC12 cells in a dose-dependent manner. Treatment with the PPARγ antagonist GW9662 or PPARγ small interfering RNA counteracted the protective effect of pioglitazone on PC12 cells to different extents (P<0.01). Therefore, the present study reported the role of PPARγ in protecting PC12 cells against oxidative stress injury, which may lead to novel therapeutic approaches for neurodegenerative diseases. D.A. Spandidos 2023-09-22 /pmc/articles/PMC10580242/ /pubmed/37854503 http://dx.doi.org/10.3892/etm.2023.12221 Text en Copyright: © Li et al. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Li, Yali
Long, Jun
Li, Libo
Yu, Ziyao
Liang, Yanjing
Hou, Bin
Xiang, Li
Niu, Xiaolin
Pioglitazone protects PC12 cells against oxidative stress injury: An in vitro study of its antiapoptotic effects via the PPARγ pathway
title Pioglitazone protects PC12 cells against oxidative stress injury: An in vitro study of its antiapoptotic effects via the PPARγ pathway
title_full Pioglitazone protects PC12 cells against oxidative stress injury: An in vitro study of its antiapoptotic effects via the PPARγ pathway
title_fullStr Pioglitazone protects PC12 cells against oxidative stress injury: An in vitro study of its antiapoptotic effects via the PPARγ pathway
title_full_unstemmed Pioglitazone protects PC12 cells against oxidative stress injury: An in vitro study of its antiapoptotic effects via the PPARγ pathway
title_short Pioglitazone protects PC12 cells against oxidative stress injury: An in vitro study of its antiapoptotic effects via the PPARγ pathway
title_sort pioglitazone protects pc12 cells against oxidative stress injury: an in vitro study of its antiapoptotic effects via the pparγ pathway
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10580242/
https://www.ncbi.nlm.nih.gov/pubmed/37854503
http://dx.doi.org/10.3892/etm.2023.12221
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