Mdivi‑1 attenuates sodium azide‑induced apoptosis in H9c2 cardiac muscle cells

Xu,Xuehua; Luo,Chengliang; Zhang,Zhixiang; Hu,Jun; Gao,Xiangting; Zuo,Yuanyi; Wang,Yun; Zhu,Shaohua

doi:10.3892/mmr.2017.7359

Mdivi‑1 attenuates sodium azide‑induced apoptosis in H9c2 cardiac muscle cells

Authors:
- Xuehua Xu
- Chengliang Luo
- Zhixiang Zhang
- Jun Hu
- Xiangting Gao
- Yuanyi Zuo
- Yun Wang
- Shaohua Zhu
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Affiliations: Department of Forensic Medicine, Medical College of Soochow University, Suzhou, Jiangsu 215123, P.R. China
Published online on: August 24, 2017 https://doi.org/10.3892/mmr.2017.7359
Pages: 5972-5978
Copyright: © Xu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The aim of the current study was to investigate the effect of mitochondrial division inhibitor 1 (Mdivi‑1) in sodium azide‑induced cell death in H9c2 cardiac muscle cells. Mdivi‑1 is a key inhibitor of the mitochondrial division protein dynamin‑related protein 1 (Drp1). Mdivi‑1 was added to H9c2 cells for 3 h, after which, the cells were treated with sodium azide for 24 h. Cell viability was measured by Cell Counting kit‑8 assay. DAPI staining was used to observe nuclear morphology changes by microscopy. To further investigate the role of mitochondria in sodium azide‑induced cell death, mitochondrial membrane potential (ΔΨm) and the cellular ATP content were determined by JC‑1 staining and ATP‑dependent bioluminescence assay, respectively. Reactive oxygen species (ROS) production was also assessed by use of the specific probe 2',7'‑dichlorodihydrofluorescein diacetate. In addition, the expression of Drp1 and of the apoptosis‑related proteins BCL2 apoptosis regulator (Bcl‑2), and BCL2 associated X (Bax) was determined by western blotting. The present findings demonstrated that pretreatment with Mdivi‑1 attenuated sodium azide‑induced H9c2 cell death. Mdivi‑1 pretreatment also inhibited the sodium azide‑induced downregulation of Bcl‑2 expression and upregulation of Bax and Drp1 expression. In addition, the mitochondrion was revealed to be the target organelle of sodium azide‑induced toxicity in H9c2 cells. Mdivi‑1 pretreatment moderated the dissipation of ΔΨm, preserved the cellular ATP contents and suppressed the production of ROS. The results suggested that the mechanism of sodium azide‑induced cell death in H9c2 cells may involve the mitochondria‑dependent apoptotic pathway. The present results indicated that Mdivi‑1 may have a cardioprotective effect against sodium azide‑induced apoptosis in H9c2 cardiac muscle cells.

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