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电压依赖性阴离子通道介导难治性癫痫中的细胞凋亡。

Voltage-dependent anion channels mediated apoptosis in refractory epilepsy.

作者信息

Zhao Yan, Jiang Wen-Jing, Ma Lin, Lin Yan, Wang Xing-Bang

机构信息

Department of Geriatric Medicine, Shandong Key Laboratory of Cardiovascular Proteomics, Qilu Hospital of Shandong University, Jinan, 250012, Shandong Province, China.

Department of Neurology, Qilu Hospital of Shandong University, Jinan, 250012, Shandong Province, China.

出版信息

Open Med (Wars). 2020 Aug 3;15(1):745-753. doi: 10.1515/med-2020-0113. eCollection 2020.

Abstract

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 , 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 . 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.

摘要

本研究的目的是探讨电压依赖性阴离子通道(VDAC)在难治性癫痫神经元线粒体介导的凋亡中的作用。进行蛋白质免疫印迹分析以检测细胞色素c、半胱天冬酶9、Bax和Bcl-2的变化。还进行了TUNEL检测,以研究在有或没有Bax或Bcl-2的情况下,VDAC1上调和下调时的细胞凋亡情况。VDAC1诱导Bax、Bcl-2和半胱天冬酶9,增加细胞色素c的释放。VDAC1在难治性癫痫的凋亡性细胞死亡中起重要作用。得出结论,VDAC1在难治性癫痫中起重要作用,可能是抗癫痫药物的一个潜在治疗靶点。本研究为难治性癫痫的可能机制提供了新的认识。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7da6/7712518/faba81e40a99/j_med-2020-0113-fig001.jpg

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