Abstract
Diaphragm dysfunction is an important clinical problem worldwide. Hydrogen sulfide (H2S) is involved in many physiological and pathological processes in mammals. However, the effect and mechanism of H2S in diaphragm dysfunction have not been fully elucidated. In this study, we detected that the level of H2S was decreased in lipopolysaccharide- (LPS-) treated L6 cells. Treatment with H2S increased the proliferation and viability of LPS-treated L6 cells. We found that H2S decreased reactive oxygen species- (ROS-) induced apoptosis through the mitogen-activated protein kinase (MAPK) signaling pathway in LPS-treated L6 cells. Administration of H2S alleviated LPS-induced inflammation by mediating the toll-like receptor-4 (TLR-4)/nuclear factor-kappa B (NF-κB) signaling pathway in L6 cells. Furthermore, H2S improved diaphragmatic function and structure through the reduction of inflammation and apoptosis in the diaphragm of septic rats. In conclusion, these findings indicate that H2S ameliorates LPS-induced diaphragm dysfunction in rats by reducing apoptosis and inflammation through ROS/MAPK and TLR4/NF-κB signaling pathways. Novel slow-releasing H2S donors can be designed and applied for the treatment of diaphragm dysfunction.
Highlights
The diaphragm is a dome-shaped skeletal muscle in mammals that is mainly required for respiratory function [1, 2]
The levels of H2S in LPS-treated L6 cells, as well as in the supernatant, were lower than those in untreated L6 cells and the supernatant (Figures 1(e) and 1(f)). These results suggest that H2S may play an important role in the growth of L6 cells
L6 cells were used to evaluate the effects of H2S on the LPS-induced diaphragmatic injury in vitro
Summary
The diaphragm is a dome-shaped skeletal muscle in mammals that is mainly required for respiratory function [1, 2]. Diaphragm dysfunction is involved in a number of clinical conditions, including interstitial lung disease, chronic obstructive pulmonary disease, heart failure, spinal cord injury, critical illness and mechanical ventilation, and neuromuscular disease [4,5,6,7,8,9]. An increasing number of studies indicate that diaphragm dysfunction has been linked to Oxidative Medicine and Cellular Longevity impaired exercise tolerance, increased breathlessness, prolonged and difficult weaning from mechanical ventilation, and adverse health outcomes [10,11,12]. The effect and mechanism of H2S in diaphragm dysfunction have not been fully elucidated
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