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Published on: January 11, 2019
Mdivi‑1 attenuates sodium azide‑induced apoptosis in H9c2 cardiac muscle cells
Xuehua Xu1, Chengliang Luo1, Zhixiang Zhang1
1Department of Forensic Medicine, Medical College of Soochow University, Suzhou, Jiangsu 215123, P.R. China.
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.
Insights
Mitochondrial division inhibitor 1 (Mdivi-1) protects H9c2 cardiac cells from sodium azide-induced death. Mdivi-1 preserves mitochondrial function and reduces oxidative stress, suggesting a cardioprotective effect.
Area of Science:
- Cardiology
- Cell Biology
- Biochemistry
Background:
- Sodium azide induces cell death in H9c2 cardiac muscle cells.
- Mitochondrial dysfunction plays a critical role in this cell death pathway.
- Dynamin-related protein 1 (Drp1) is involved in mitochondrial dynamics and apoptosis.
Purpose of the Study:
- To investigate the protective effect of mitochondrial division inhibitor 1 (Mdivi-1) against sodium azide-induced cell death in H9c2 cells.
- To elucidate the role of mitochondria and Drp1 in sodium azide toxicity.
- To assess the potential cardioprotective mechanism of Mdivi-1.
Main Methods:
- H9c2 cells were pretreated with Mdivi-1 before sodium azide exposure.
- Cell viability was assessed using the Cell Counting kit-8 assay.
- Mitochondrial membrane potential (ΔΨm), ATP content, reactive oxygen species (ROS) production, and protein expression (Drp1, Bcl-2, Bax) were measured.
Main Results:
- Mdivi-1 pretreatment significantly attenuated sodium azide-induced H9c2 cell death.
- Mdivi-1 inhibited the downregulation of Bcl-2 and upregulation of Bax and Drp1 induced by sodium azide.
- Mdivi-1 preserved ΔΨm, maintained cellular ATP levels, and suppressed ROS production.
Conclusions:
- Sodium azide induces H9c2 cell death primarily through a mitochondria-dependent apoptotic pathway.
- Mdivi-1 exhibits a cardioprotective effect by inhibiting Drp1, preserving mitochondrial function, and reducing oxidative stress.
- Mdivi-1 demonstrates potential as a therapeutic agent against cardiac injury.
