Hydrogen Sulfide Protects against Chemical Hypoxia-Induced Injury via Attenuation of ROS-Mediated Ca(2+) Overload and Mitochondrial Dysfunction in Human Bronchial Epithelial Cells

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 H(2)S on CoCl(2)-induced cell injury in 16HBE14o- cells. The effect of CoCl(2) 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 μmol/L) of CoCl(2) (a common chemical mimic of hypoxia) was measured by using fluorescent probe DCFH-DA. It was shown that, in 16HBE14o- cells, CoCl(2) acutely increased the ROS content in a dose-dependent manner, and the increased ROS was inhibited by the NaHS (as a donor of H(2)S). Moreover, the calcium ion fluorescence probe Fura-2/AM and fluorescence dye Rh123 were used to investigate the intracellular calcium concentration ([Ca(2+)](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 CoCl(2) effectively elevated the Ca(2+) influx, declined the MMP, and aggravated apoptosis, which were abrogated by NaHS. These results demonstrate that H(2)S could attenuate CoCl(2)-induced hypoxia injury via reducing ROS to perform an agonistic role for the Ca(2+) influx and MMP dissipation.