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Voltage-dependent anion channels mediated apoptosis in refractory epilepsy
The purpose of this study was to investigate the role of voltage-dependent anion channel (VDAC) in mitochondria-mediated apoptosis of neurons in refractory epilepsy. Western blot analyses were carried out to detect the changes in cytochrome C, caspase 9, Bax, and Bcl-2. TUNEL assays were also carrie...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
De Gruyter
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7712518/ https://www.ncbi.nlm.nih.gov/pubmed/33336032 http://dx.doi.org/10.1515/med-2020-0113 |
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author | Zhao, Yan Jiang, Wen-Jing Ma, Lin Lin, Yan Wang, Xing-Bang |
author_facet | Zhao, Yan Jiang, Wen-Jing Ma, Lin Lin, Yan Wang, Xing-Bang |
author_sort | Zhao, Yan |
collection | PubMed |
description | The purpose of this study was to investigate the role of voltage-dependent anion channel (VDAC) in mitochondria-mediated apoptosis of neurons in refractory epilepsy. Western blot analyses were carried out to detect the changes in cytochrome C, caspase 9, Bax, and Bcl-2. TUNEL assays were also carried out to investigate cell apoptosis under the upregulation and downregulation of VDAC1 with or without Bax or Bcl-2. VDAC1 induced Bax, Bcl-2, and caspase 9, increasing the release of cytochrome C. VDAC1 played an essential role in the apoptotic cell death of refractory epilepsy. It is concluded that VDAC1 plays an important role in refractory epilepsy and could be a possible therapeutic target of anti-epileptic drugs. The current study provides a new understanding of the possible mechanisms of refractory epilepsy. |
format | Online Article Text |
id | pubmed-7712518 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | De Gruyter |
record_format | MEDLINE/PubMed |
spelling | pubmed-77125182020-12-16 Voltage-dependent anion channels mediated apoptosis in refractory epilepsy Zhao, Yan Jiang, Wen-Jing Ma, Lin Lin, Yan Wang, Xing-Bang Open Med (Wars) Research Article The purpose of this study was to investigate the role of voltage-dependent anion channel (VDAC) in mitochondria-mediated apoptosis of neurons in refractory epilepsy. Western blot analyses were carried out to detect the changes in cytochrome C, caspase 9, Bax, and Bcl-2. TUNEL assays were also carried out to investigate cell apoptosis under the upregulation and downregulation of VDAC1 with or without Bax or Bcl-2. VDAC1 induced Bax, Bcl-2, and caspase 9, increasing the release of cytochrome C. VDAC1 played an essential role in the apoptotic cell death of refractory epilepsy. It is concluded that VDAC1 plays an important role in refractory epilepsy and could be a possible therapeutic target of anti-epileptic drugs. The current study provides a new understanding of the possible mechanisms of refractory epilepsy. De Gruyter 2020-08-03 /pmc/articles/PMC7712518/ /pubmed/33336032 http://dx.doi.org/10.1515/med-2020-0113 Text en © 2020 Yan Zhao et al., published by De Gruyter http://creativecommons.org/licenses/by/4.0 This work is licensed under the Creative Commons Attribution 4.0 International License. |
spellingShingle | Research Article Zhao, Yan Jiang, Wen-Jing Ma, Lin Lin, Yan Wang, Xing-Bang Voltage-dependent anion channels mediated apoptosis in refractory epilepsy |
title | Voltage-dependent anion channels mediated apoptosis in refractory epilepsy |
title_full | Voltage-dependent anion channels mediated apoptosis in refractory epilepsy |
title_fullStr | Voltage-dependent anion channels mediated apoptosis in refractory epilepsy |
title_full_unstemmed | Voltage-dependent anion channels mediated apoptosis in refractory epilepsy |
title_short | Voltage-dependent anion channels mediated apoptosis in refractory epilepsy |
title_sort | voltage-dependent anion channels mediated apoptosis in refractory epilepsy |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7712518/ https://www.ncbi.nlm.nih.gov/pubmed/33336032 http://dx.doi.org/10.1515/med-2020-0113 |
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