1. Hydrogen Sulfide Protects against Chemical Hypoxia-Induced Injury via Attenuation of ROS-Mediated Ca 2+ Overload and Mitochondrial Dysfunction in Human Bronchial Epithelial Cells.
- Author
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Liu CX, Tan YR, Xiang Y, Liu C, Liu XA, and Qin XQ
- Subjects
- Bronchi pathology, Cell Hypoxia drug effects, Cell Line, Transformed, Epithelial Cells pathology, Humans, Membrane Potential, Mitochondrial drug effects, Mitochondria pathology, Bronchi metabolism, Calcium metabolism, Epithelial Cells metabolism, Hydrogen Sulfide pharmacology, Mitochondria metabolism, Reactive Oxygen Species metabolism
- Abstract
Oxidative stress induced by hypoxia/ischemia resulted in the excessive reactive oxygen species (ROS) and the relative inadequate antioxidants. As the initial barrier to environmental pollutants and allergic stimuli, airway epithelial cell is vulnerable to oxidative stress. In recent years, the antioxidant effect of hydrogen sulfide (H
2 S) has attracted much attention. Therefore, in this study, we explored the impact of H2 S on CoCl2 -induced cell injury in 16HBE14o- cells. The effect of CoCl2 on the cell viability was detected by Cell Counting Kit (CCK-8) and the level of ROS in 16HBE14o- cells in response to varying doses (100-1000 μ mol/L) of CoCl2 (a common chemical mimic of hypoxia) was measured by using fluorescent probe DCFH-DA. It was shown that, in 16HBE14o- cells, CoCl2 acutely increased the ROS content in a dose-dependent manner, and the increased ROS was inhibited by the NaHS (as a donor of H2 S). Moreover, the calcium ion fluorescence probe Fura-2/AM and fluorescence dye Rh123 were used to investigate the intracellular calcium concentration ([Ca2+ ]i ) and mitochondria membrane potential (MMP) in 16HBE14o- cells, respectively. In addition, we examined apoptosis of 16HBE14o- cells with Hoechst 33342. The results showed that the CoCl2 effectively elevated the Ca2+ influx, declined the MMP, and aggravated apoptosis, which were abrogated by NaHS. These results demonstrate that H2 S could attenuate CoCl2 -induced hypoxia injury via reducing ROS to perform an agonistic role for the Ca2+ influx and MMP dissipation.- Published
- 2018
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