Hydrogen Sulfide Protects against Chemical Hypoxia-Induced Injury via Attenuation of ROS-Mediated Ca²⁺Overload and Mitochondrial Dysfunction in Human Bronchial Epithelial Cells

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 (H2S) has attracted much attention. Therefore, in this study, we explored the impact of H2S 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 μmol/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 H2S). 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 H2S could attenuate CoCl2-induced hypoxia injury via reducing ROS to perform an agonistic role for the Ca2+ influx and MMP dissipation.

Hydrogen sulfide attenuates cigarette smoke-induced airway remodeling by upregulating SIRT1 signaling pathway

“…For instance, H 2 S can reduce the production and accumulation of ROS and NOX2 in the lung after acute lung injury [46]. H 2 S protected human bronchial epithelial cells against chemical hypoxia-induced injury via attenuation of ROS-mediated Ca 2+ overload [47]. ROS can activate a wide variety of remodeling signaling kinases and transcription factors, which play a central role in the occurrence and development of bronchial remodeling.…”

Hydrogen sulfide, oxygen, and calcium regulation in developing human airway smooth muscle

“…In mice, absence of CSE expression promotes AHR. 29 Exogenous administration of H 2 S has been demonstrated as protective in ventilator-induced lung injury, 68,69 acute lung injury, [70][71][72][73][74] hypoxia/hyperoxia environments, [74][75][76] and during acute viral illnesses. [77][78][79] Compared to these data, there is currently no information on H 2 S in the developing bronchial airways per se.…”

Extrinsic factors influencing gut microbes, the immediate consequences and restoring eubiosis

“…The stress induced by ROS production defined as oxidative stress. Oxidative stress consist of biological system for the process of detoxification and secondary damage repair (Liu et al 2018 ). The new study though not supported with enough literature is the potential role of heat shock proteins (HSPs) in the pathogenesis of IBD.…”